7.3.10 Hepato-splanchnic function

 Hepato-splanchnic circulation receives 30% of cardiac output and consumes 30% of the oxygen. In the event of haemodynamic failure, this organ is subject to strong vasoconstriction, designed to divert circulating volume to heart and brain [11]. Selfregulation, managed by secretion of vasoconstrictor endothelin and vasodilator NO, only functions during digestion; it is non-existent when fasting or on bypass. The portal vascular system is pressure-dependent, and the hepatic artery contributes to only 20% of hepatic blood flow. The flow of the portal vein and the hepatic artery are correlated, so that venous stasis, e.g. due to malposition of the venous cannula, results in a decrease in portal flow but a compensatory increase in hepatic artery flow [9]. 

Any significant alteration in perfusion pressure or pump rate may lead to periods of hepatic ischaemia. Even without incident, ECC influences liver function. Hyperbilirubinemia, transient enzyme elevation and a momentary decrease in lactate metabolism are common after ECC and recover within a few days [3]. On the other hand, alterations in liver function are proportional to the circulating values of C3a and C4a fractions of complement, and thus to the intensity of the systemic inflammatory response [8]. Various factors predict the extent of this postoperative liver disturbance [3].

  • Pre-existing liver damage; patients in Child A category have a morbidity of 40% and a mortality of 11%, but those in Child B and Child C stages have a mortality of 18% and 67% respectively [4,7];
  • Systemic stasis: high CVP on LV failure, PAH, tricuspid regurgitation;
  • Intraoperative low flow (use of alpha catecholamines);
  • Blocking of the suprahepatic venous return through the venous cannula of the ECC;
  • Long lasting ECC [5].

The incidence of liver failure after cardiac surgery is low (0.1%), but its mortality exceeds 50% [3]. It is related to the triple mechanism of hepatic ischaemia, stasis liver and inflammatory/medicinal reaction.

The adequacy of splanchnic perfusion to the needs of the digestive tract is generally achieved in hypothermia, but not necessarily during rewarming.  In fact  the drop in pHi is most marked during normothermia [2]. The length of the bypass, possible hypotension, local acidosis, flow depulsation and systemic inflammatory syndrome all contribute to increased permeability of the digestive mucosa [12]. Although the incidence of GI complications is low after CABG (0.6-3% of cases), conjugated hyperbilirubinemia occurs in 20-35% of operated patients . Digestive hyperpermeability leads to endotoxin translocation in 10-55% of patients [1,10]. The latter contributes to multivisceral failure and severe postoperative sepsis. In addition, episodes of digestive acidosis (low pHi) occur between the third and fifth hour after ECC in over 50% of patients [6].

Unfortunately, there is no real prophylaxis for post-ECC liver failure. But some measures tend to reduce the incidence of this complication [3].

  • Decrease the duration of ECC (< 70 minutes).
  • Maintain normal blood flow (2.4 L/min/m2 ) and MAP > 60 mmHg.
  • Keep the PVC as low as possible.
  • Maintain moderate hypothermia (32°C).
  • Avoid haemodilution (Ht > 28%) because of the hypoalbuminemia already present in patients; limit infusions and transfusions.
  • Avoid highly metabolised halogens (halothane 20-40%, sevoflurane 4%, enflurane 3%); the lowest metabolised are isoflurane (0.2%) and desflurane (0.02%). A preconditioning effect has been described in liver surgery. Avoid diazepines.
  • Decreased metabolism extends the effect of drugs with high hepatic extraction (fentanils, morphine). Remifentanil, atracurium and cisatracurium have the advantage of being metabolised by serum esterases; propofol infusion is well suited.
  • Low dose dobutamine or milrinone infusion.
  • Maintain normal SAR and avoid alpha vasoconstrictors; adrenaline and vasopressin decrease splanchnic flow. Hepatic haemodynamics are best maintained by dobutamine.
  • Phosphodiesterase 3 inhibitors (milrinone) and levosimendan increase splanchnic flow, but the protective effect of continuous infusion of dopamine or dopexamine remains unclear.

 

 Liver function 
 Apart from avoiding any hepatotoxic substances, the only protection is the maintenance of normal haemodynamics without the use of alpha vasoconstrictor.

 

© CHASSOT PG, GRONCHI F, April 2008, last update, December 2019

 

References

  1. AOUIFI A, PIRIOU V, BASTIEN O, et al. Severe digestive complications after heart surgery using extracorporeal circulation. Can J Anaesth 1999; 46:114-21
  2. CROUGHWELL ND, NEWMAN NF, LOWRY E, et al. Effect of temperature during cardiopulmonary bypasson gastric mucosal perfusion. Br J Anaesth 1997; 78:34-8
  3. DI TOMASSO N, MONACO F, LANDONI G. Hepatic and renal effects of cardiopulmonary bypass. Best Pract Res Clin Anaesthesiol 2015; 29:151-61
  4. HAYASHIDA N, SHOUJIMA T, TESHIMA H, et al. Clinical outcomes after cardiac operations in patients with cirrhosis. Ann Thorac Surg 2004; 77:500-5
  5. KUMLE B, BOLDT J, SUTTNER SW, et al. Influence of prolonged cardiopulmonary bypass times on splanchnic perfusion and markers of splanchnic organ function. Ann Thorac Surg 2003; 75:1558-64
  6. MYTHEN MG, WEBB AR. Perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 1995; 130:423-9
  7. NOBUHIKO  H, TAKAHIRO S, HIDEKI T, et al. Clinical outcome after cardiac operations in patients with cirrhosis. Ann Thorac Surg 2004; 77:500-5
  8. NOMOTO S, SHIMAHARA Y, KUMADA K, et al. Influence of hepatic mitochondrial redox state on complement biosynthesis and activation during and after cardiopulmonary bypass operations. Eur J Cardiothorac Surg 1996; 10:273-8
  9. PANNEN BH. New insights into the regulation of hepatic blood flow after ischemia and reperfusion. Anesth Analg 2002; 94:1448-57
  10. RIDDINGTON DW, VENKATESH B, BOIVIN CM, et al. Intestinal permeability, gastric intramucosal pH, and systemic endotoxemia in patients undergoing cardiopulmonary bypass. JAMA 1996; 275:1007-12
  11. ROUGE P, BUYS S. ECC and hepato-planchnic circulation. In: JANVIER G, LEHOT JJ (ed). Circulation extracorporelle: principes et pratique, 2nd edition. Paris, Arnette Groupe Liaison SA, 2004, pp 363-75
  12. SINCLAIR DG, HASLAM PL, QUINLAN GJ, et al. The effect of cardiopulmonary bypass on intestinal and pulmonary endothelial permeability. Chest 1995; 108:718-24