Pediatric Anesthesia: Case Report
Patients with hypoplastic left heart syndrome (HLHS) and other single ventricle lesions are surgically palliated shortly after birth with the Norwood procedure (1,2). The right ventricle functions as the systemic ventricle, and pulmonary blood flow (Qp) is provided by either a Blalock-Taussig shunt or a right ventricle to pulmonary artery conduit (modified Norwood). The ratio of pulmonary to systemic blood flow, or Qp/Qs, depends on the balance between systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). PVR is affected by changes in Paco2, Pao2, acid-base status, body temperature, and lung volumes (1,3). Laparoscopic surgery in these patients is concerning because the increase in intraabdominal pressure (IAP) and Paco2 from the capnoperitoneum decreases cardiac index (CI) and increases PVR, which can potentially lead to hypoxemia and hypotension (4,5). However, laparoscopy results in less postoperative pain and pulmonary dysfunction with shorter hospital stays compared with open surgery (6,7). Patients with HLHS develop comorbid conditions, such as gastroesophageal reflux disease, requiring surgical correction. We discuss the anesthetic implications during laparoscopic Nissen fundoplication for a series of five infants with palliated HLHS.
After IRB approval, the records of infants who had undergone laparoscopic Nissen fundoplication with gastrostomy tube placement after modified Norwood for HLHS were reviewed (Table 1). The mean time interval between modified Norwood and fundoplication was 38 ± 6 days. Preoperative medications included angiotensin-converting enzyme inhibitors, digoxin, and diuretics. Anesthesia was induced with IV ketamine or etomidate, fentanyl, and rocuronium before tracheal intubation. A second IV and an arterial catheter were inserted. Temperature was monitored rectally and maintained with a forced air warmer. Antibiotics were administered for endocarditis prophylaxis. The stomach was decompressed with an orogastric tube before Veress needle insertion. The peritoneum was insufflated with CO2 to a maximum pressure of 12 mm Hg at low flow (1 L/min). After trocar placement, the patient was positioned in 30° reverse Trendelenburg position for optimal surgical exposure. Anesthesia was maintained with fentanyl (5–17 μg/kg), rocuronium, and isoflurane at 1 minimum alveolar concentration in oxygen/air (Fio2, 0.21–0.40). Arterial blood gases were checked at regular intervals to monitor for acidosis and hypercarbia (Fig. 1). Pressure control ventilation was used to avoid high peak inspiratory pressure, and minute ventilation was increased to maintain normocarbia. Patients received red blood cell transfusions to keep the hematocrit more than 40% according to our institutional practice. Two patients empirically received small-dose dopamine or dobutamine for inotropic support during insufflation. All patients remained hemodynamically stable (Fig. 2). After surgery, inotropes were discontinued and patients were admitted to the cardiovascular intensive care unit (CVICU). All patients were tracheally extubated by postoperative day 1. There were no intraoperative or postoperative complications.
Laparoscopic Nissen fundoplication can be safely performed in patients with HLHS with proper monitoring and postoperative ICU care. The laparoscopic approach may be the preferred technique in these patients because of decreased postoperative pulmonary dysfunction (8).
In patients with HLHS undergoing laparoscopic fundoplication, arterial catheter placement should be considered in addition to standard noninvasive monitors. As CO2 retention and acidosis negatively impact Qp and PVR, frequent arterial blood gas sampling is recommended (9). End-tidal CO2 monitoring correlates poorly with Paco2 during peritoneal insufflation particularly in patients with cyanotic heart disease (10,11). Early detection and corrective measures are critical in this high-risk subgroup because persistent respiratory acidosis can result in reduced Qp and systemic hypoxemia.
Avoiding hypercarbia requires an effective ventilation strategy. The pneumoperitoneum limits diaphragmatic excursion and decreases pulmonary compliance (9,12,13). Absorption of CO2 can be significant, and an increase in minute ventilation is required to maintain normocarbia (12,14,15). Prevention of atelectasis with an adequate tidal volume and positive end-expiratory pressure preserves functional residual capacity (16). Inspired oxygen concentration should be the minimum necessary to achieve baseline oxygen saturation. Hyperoxia decreases PVR, leading to pulmonary overcirculation and decreased systemic perfusion. Nitrous oxide is avoided because of the risk of air embolism. Bowel distension from nitrous oxide causing interference with surgical exposure was insignificant in a previous study (17).
Hemodynamic changes from pneumoperitoneum warrant consideration. SVR increases and CI decreases especially in the reverse Trendelenburg position from decreased venous return (18,19). A study using transesophageal echocardiography during pediatric laparoscopy has shown that CI decreases approximately 13% at an IAP of 12 mm Hg in healthy children with no adverse effects at an IAP of 6 mm Hg (20). Because decreased CI may reduce shunt flow, resulting in desaturation, a maximum IAP of 12 mm Hg has been recommended for patients with cardiac disease (16). The right ventricle to pulmonary artery conduit modification better preserves diastolic blood pressure and may allow patients with palliated HLHS to tolerate the hemodynamic changes associated with peritoneal insufflation (2).
In conclusion, although patients with palliated HLHS are a high-risk cohort, laparoscopic Nissen fundoplication can be safely performed. We recommend careful hemodynamic monitoring and admission to the ICU for postoperative observation.
1. Norwood WI. Hypoplastic left heart syndrome. Cardiol Clin 1989;7:377–85.
2. Pizarro C, Malec E, Maher KO, et al. Right ventricle to pulmonary artery conduit improves outcome after stage I Norwood for hypoplastic left heart syndrome. Circulation 2003;108 Suppl 1:II155–60.
3. Schwartz SM, Dent CL, Musa NL, Nelson DP. Single-ventricle physiology. Crit Care Clin 2003;19:393–411.
4. Manner T, Aantaa R, Alanen M. Lung compliance during laparoscopic surgery in paediatric patients. Paediatr Anaesth 1998;8:25–9.
5. Halachmi S, El-Ghoneimi A, Bissonnette B, et al. Hemodynamic and respiratory effect of pediatric urological laparoscopic surgery: A retrospective study. J Urol 2003;170:1651–4.
6. Pessaux P, Arnaud JP, Ghavami B, et al. Morbidity of laparoscopic fundoplication for gastroesophageal reflux: A retrospective study about 1470 patients. Hepatogastroenterology 2002;49:447–50.
7. Collins JB 3rd, Georgeson KE, Vicente Y, Hardin WD Jr. Comparison of open and laparoscopic gastrostomy and fundoplication in 120 patients. J Pediatr Surg 1995;30:1065–70.
8. Powers CJ, Levitt MA, Tantoco J, et al. The respiratory advantage of laparoscopic Nissen fundoplication. J Pediatr Surg 2003;38:886–91.
9. Kendall AP, Bhatt S, Oh TE. Pulmonary consequences of carbon dioxide insufflation for laparoscopic cholecystectomies. Anaesthesia 1995;50:286–9.
10. Wulkan ML, Vasudevan SA. Is end-tidal CO2 an accurate measure of arterial CO2 during laparoscopic procedures in children and neonates with cyanotic congenital heart disease? J Pediatr Surg 2001;36:1234–6.
11. Hirvonen EA, Nuutinen LS, Kauko M. Ventilatory effects, blood gas changes, and oxygen consumption during laparoscopic hysterectomy. Anesth Analg 1995;80:961–6.
12. Petrat G, Weyandt D, Klein U. Anesthetic considerations in pediatric laparoscopic and thoracoscopic surgery. Eur J Pediatr Surg 1999;9:282–5.
13. Rowney DA, Aldridge LM. Laparoscopic fundoplication in children: Anaesthetic experience of 51 cases. Paediatr Anaesth 2000;10:291–6.
14. Walsh MT, Vetter TR. Anesthesia for pediatric laparoscopic cholecystectomy. J Clin Anesth 1992;4:406–8.
15. Puri GD, Singh H. Ventilatory effects of laparoscopy under general anaesthesia. Br J Anaesth 1992;68:211–3.
16. Pennant JH. Anesthesia for laparoscopy in the pediatric patient. Anesthesiol Clin North America 2001;19:69–88.
17. Taylor E, Feinstein R, White PF, Soper N. Anesthesia for laparoscopic cholecystectomy: Is nitrous oxide contraindicated? Anesthesiology 1992;76:541–3.
18. Joris JL, Noirot DP, Legrand MJ, et al. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993;76:1067–71.
19. Hein HA, Joshi GP, Ramsay MA, et al. Hemodynamic changes during laparoscopic cholecystectomy in patients with severe cardiac disease. J Clin Anesth 1997;9:261–5.
20. Sakka SG, Huettemann E, Petrat G, et al. Transoesophageal echocardiographic assessment of haemodynamic changes during laparoscopic herniorrhaphy in small children. Br J Anaesth 2000;84:330–4.