Hypercarbia causes hemodynamic changes in the brain, such as cerebral vasodilation, increased cerebral blood flow (CBF), and increased intracranial pressure (ICP) [5]. These effects are only partially reversed with anesthesia-induced hyperventilation [4]. When ETCO₂ is kept relatively constant, CBF still increases, suggesting an additional neurohormonal factor [20]. Karsli et al. found that the middle cerebral artery blood flow velocity increased proportionally to the mean arterial pressure (MAP) and ETCO₂ during the first 8 min of pneumoperitoneum, while HR remained the same [19]. After 20 min, ETCO₂ continued to increase, whereas the middle cerebral artery blood flow velocity and MAP reached a plateau and then decreased progressively. Conversely, during retroperitoneoscopy, both CBF velocity and ETCO₂ increase progressively throughout the procedure but show parallel decreases towards baseline within 5 min of desufflation. It therefore seems that CBF and ETCO₂ increase more gradually during retroperitoneal insufflation, compared to the more rapid increase and plateau effect observed during pneumoperitoneum. It is hypothesized, again, that this is due to the smaller absorptive surface of the retroperitoneum and absence of the peritoneal barrier which induces the plateau effect eventually [19]. These changes may have no clinical sequelae except in long cases, where the anesthetist and the surgeon should be aware of differential absorption rates depending on the approach.

Absorbed CO₂ imposes an increased load on the respiratory system also, where hypercarbia and respiratory acidosis can result. ETCO₂ is often used as a surrogate measure of absorbed CO₂. Increases in ETCO₂ are noted up to 33 % over baseline values despite ventilator adjustments in one study examining both thoracoscopy and laparoscopy in neonates [4, 8]. To clear excess CO₂ and maintain normocarbia, minute ventilation may need to be increased by up to 50–75 % along with intermittent positive pressure ventilation [7]. Studies in neonates found that an increase of 22.6–40 % in minute ventilation with positive airway pressure was needed to help restore normocarbia [8, 21]. Indeed, Bannister observed that 95 % of patients required at least one ventilator adjustment during surgery to restore ETCO₂ to within 10 % of their baseline value [2].

During prolonged procedures, large amounts of CO₂ are also buffered in the muscle and fat, which must be eliminated by the lungs postoperatively [7]. Respiratory acidosis can persist postoperatively in conditions of poor respiratory function or when respiratory drive remains suppressed [7]. Overall, however, when compared to traditional open surgery, the postoperative respiratory benefits of MIS, such as improved rates of extubation and shorter chest physiotherapy requirements, likely outweigh the physiologic changes observed during laparoscopy [3].

CO₂ absorption independently influences cardiac function with its direct depressive effects on the myocardium and secondary effects mediated by the autonomic nervous system. In adults, catecholamine release helps maintain CO by increasing HR and stroke volume (SV), which counteracts the effects of increased IAP [5, 22]. Hypercarbia similarly counteracts some of the effects of increased IAP by decreasing SVR and potentiating tachyarrhythmias, unlike the possible bradycardia that can occur with insufflation [7, 22]. Overall, these changes are well tolerated, and the compensatory ability improves with increasing age and size of children.

Increased IAP may affect the perfusion dynamics of the brain by causing a prompt and sustained increase in intracranial pressure (ICP) due to decreased jugular venous return. This finding is enhanced by the vasodilatory effects that occur with CO₂ absorption. Intracranial venous stasis causes decreased resorption and drainage of cerebrospinal fluid, thereby increasing ICP further. Overall, these effects are proportional to the degree of IAP [4].

Two animal studies have evaluated the effects of increased IAP on ICP [24, 25]. Josephs et al. found that at an IAP of 15 mmHg, ICP increased from 13 to 18.7 mmHg, independently of arterial pH and CO₂ levels. Bloomfield et al. found that an IAP of 25 mmHg increased ICP from a mean of 7.6–21.4 mmHg. Cerebral perfusion pressure fell from 82 to 62 mmHg but was partially restored with volume expansion. The implications of these findings in normal children are unclear, but extra caution should be used in conditions of decreased intracranial compliance, such as head injuries and ventriculoperitoneal (VP) shunts.

In otherwise healthy children, VP shunts are not currently considered an absolute contraindication to pneumoperitoneum [4]. If there are presumed risks in this population, such as shunt malfunction, infection, retrograde flow, or pneumocephalus, then protective means that include clamping or exteriorizing the shunt, shielding the shunt in an endoscopic bag, or regular exsufflation with pumping of the reservoir may be implemented [26–29]. Uzzo et al. advocated invasive ICP monitoring techniques and intermittent drainage of cerebrospinal fluid in their description of two pediatric cases of laparoscopic bladder autoaugmentation [30]. However, the need for such techniques in healthy children with VP shunts has been questioned by others [31]. The largest series of 18 patients with VP shunts in the pediatric urology literature showed no increased clinical sequelae during major and reconstructive MIS procedures [31]. These authors suggest that the risk of invasive ICP monitoring and shunt manipulation might actually outweigh any presumed benefit and recommended routine anesthetic care as the gold standard for this population.

Data on the infection rates during laparoscopy in children are scarce. One of the largest reviews of various pediatric procedures showed no statistically significant difference in shunt infection rates when comparing open to MIS approaches [32]. With regard to the potential mechanical tubing malfunctions that may occur due to increased IAP, in vitro testing has shown that the one-way valve mechanism of the VP shunt can withstand simulated pressures of up to 80 mmHg without structural distortion [33]. More recently, testing of various VP shunt tubing mechanisms with simulated pneumoperitoneum showed no reflux during insufflation pressures of up to 25 mmHg when the tubing was filled with saline, which simulated the more realistic scenario of a functioning shunt flowing with CSF [34]. In addition to the descriptions above, a number of case reports and series have described successful laparoscopy in this population without complication, and MIS is generally considered safe and feasible with heightened awareness from the surgeon and anesthetist [26, 35–38].

The magnitude of respiratory changes from increased IAP correlates directly with the degree of pneumoperitoneum [2]. With rising IAP, the diaphragm and mediastinum are displaced more cephalad, and chest excursion is restricted. This results in decreased functional residual capacity (FRC), decreased total lung compliance, increased peak inspiratory pressure, and decreased tidal volume (TV) [4, 5, 39]. As such, the ventilation perfusion mismatch expected in routine mechanical ventilation is enhanced, and atelectasis, oxygen (O₂) desaturation, and hypercarbia can occur [2]. These effects are more pronounced in smaller children and neonates with an already low FRC and high oxygen consumption [21]. In healthy children, these changes usually have no clinical sequelae and can be counterbalanced by anesthetic adjustments. Indeed, the large majority of infants require at least one intervention by anesthesia to restore baseline TV and end tidal CO₂ (ETCO₂) [2].

With regard to retroperitoneal MIS, peak inspiratory pressures increase upon retroperitoneal space insufflation, with a resultant increase in respiratory rate and decrease in O₂ saturations [12, 40]. In their prospective evaluation of 18 children undergoing retroperitoneal laparoscopy, Lorenzo et al. found that while there was a statistically significant increase in airway pressure during retroperitoneal insufflation, there was a strong trend towards normalization after completion of the procedure [18].

The cardiovascular effects of increased IAP are complex and depend on the interplay between preload, systemic vascular resistance (SVR), and cardiac contractility [4]. Positioning and hypercarbia also independently influence these factors, and consequently the prevailing combined circumstances determine the response in each patient.