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Kidney Failure Following Liver Resection
Kidney Failure Following Liver Resection F. Saner ABSTRACT In the recent 20 years liver resection has become a routine operation with reasonably low risk. Experienced hepatobiliary centers have reported low mortality rates (0%–5%) even in series with high-risk resection (extended right or left resection). Acute kidney failure correlates well with mortality. In our series, more than 70% of patients with kidney failure, who require dialysis died. Acute renal failure develops if patients are kept hypovolemic or the patient suffers from postresectional liver failure. Herein we discuss how kidney failure following liver resection can be avoided.
L
IVER RESECTION is the only curative treatment for primary and metastatic liver tumors. Due to improved surgical techniques, as well as modern anesthesia and intensive care, this operation has become a routine procedure over the last 20 years with a reasonably low complication rate. Belghiti et al1 reported their experience in 747 liver resections with a mortality rate of 4.4%. These data were supported by another high-volume center located in Hong Kong. Poon et al2 published their experience in 1222 liver resections with a mortality rate of 4.5%. The SloanKettering Hospital (New York, NY, United States) reported a mortality of 3.1% among 1803 liver resections.3 In 2006 we recorded 322 patients following liver resections at our intensive care unit. The main diagnoses leading to liver resection were colorectal metastases (52%), followed by other metastases (20.1%) and hepatocellular carcinoma (HCC) with an incidence of 10.2%. Fifteen percent of all patients experienced a kidney injury, whereas about half of them (7.1% of all patients) required renal replacement therapy (RRT); 73% of patients who required RRT died. This observation showed the close relationship of acute renal failure in patients following liver resection, as already published in septic patients.4 There are 2 major risk factors for kidney failure in patients following liver resection: first, extensive blood loss during the operation, and second, postresectional liver failure (PRLF). Jarnagin et al3 and Imamura et al5 suggested that a blood loss of 1250 mL was a cutoff point for major complications like kidney injury. Kooby et al6 reported a significantly worse outcome even after 5 years, if the transfusion requirement exceeded 3 units of packed red cells (PRC). In the context of blood loss, the role of the central venous pressure (CVP) must be discussed: hepatobiliary surgeons rely on a low CVP (⬍5 mm Hg), as a CVP
⬎ 5 mm Hg may induce liver congestion with impaired liver outflow. Jones et al7 examined the impact of CVP on blood loss in liver resection. In this study, a CVP ⬎ 5 cm H20 (⫽ 3.75 mm Hg) induced a 5-fold greater blood loss compared with a CVP ⬍ 5 cm H20 (1000 vs 200 mL blood loss). Melendez8 from the Sloan-Kettering Hospital, New York, reported his experience in 496 liver resections whereas 38% were major liver resection (⬎ 3 segments). Guided by a special anesthesia protocol—fluid restriction, use of nitroglycerine, furosemide, systolic arterial pressure of 90 mm Hg was tolerated—the median blood loss was 645 mL. The rate of acute renal failure and RRT was only 3.1%. The hemodynamic changes in patients following liver resection are similar to those of patients with cirrhosis or acute liver failure (Fig 1).9 Depending on the remnant liver volume and on the quality of the liver (steatosis/cirrhosis), these problems will be evident. Kowalski and Abelmann10 reported in 1953 that cardiac output (CO) in cirrhotic patients was significantly higher compared with healthy volunteers. The reason for this so-called hyperdynamic state is the huge concentration of nitric oxide (NO) in the circulation, as shown in both animal11 and clinical12 trials. As a result, the cGMP concentration is increased in the splanchnic area with severe vasodilation, declining central and arterial blood volume, low pulmonary capillary wedge pressure (PCWP), low CVP, low systemic vascular resistance (SVR), increased CO, and reduced mean arterial pressure (MAP). From the Universitätsklinikum Essen, Klinik für Allgemein-, Viszeral- und Transplantationschirurgie, Essen, Germany. Address reprint requests to F. Saner, MD, Universitätsklinikum Essen, Klinik für Allgemein-, Viszeral- und Transplantationschirurgie, Hufelandstr. 55, 45 122 Essen, Germany. E-mail: fuat.saner@ uni-due.de
© 2008 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710
0041-1345/08/$–see front matter doi:10.1016/j.transproceed.2008.03.068
Transplantation Proceedings, 40, 1221–1224 (2008)
1221
1222
Fig 1. Due to increased translocation of bacteria and an impaired phagocytosis activity of the Kupffer cells in patients with liver failure an increased cytokine production is evident. Inducible nitric oxide synthase (iNOS) activity will be increased with huge amounts of nitric oxide. As a result, the cGMP concentration is increased in the splanchnic area with severe vasodilation, declining central and arterial blood volume, low pulmonary capillary wedge pressure (PCWP), low central venous pressure (CVP), low systemic vascular resistance (SVR), and increased cardiac output (CO).
The kidneys are most at risk from a pressure drop. They can maintain their blood flow in the MAP range between 80 and 120 mm Hg. If the MAP falls to ⬍80 mm Hg, there is a significant drop in the glomerular filtration rate (GFR).13 Recently, the role of CVP and blood loss has been challenged. Chhibber et al14 described no correlation between CVP and blood loss among 100 live liver donors. In a retrospective study, Schroeder et al15 compared 2 CVP policies: a low CVP group (median 3 mm Hg) and a high CVP group (median 8 mm Hg). They confirmed the data of Jones et al7 that a higher CVP induced more blood loss. However, in the low CVP group the rate of kidney injury, the requirement for dialysis, and the 30-day mortality rate were significantly higher compared with the high CVP group. Another study16 reported the effects of 3 different CVP levels on the flow velocities of the hepatic artery (HA), the portal vein (PV), and the hepatic vein (HV) in liver transplant patients. Three CVP levels (6, 8, or 9 mm Hg) were applied to the patients. There were no significant changes in flow velocities of all 3 vessels. Based on these data, the hemodynamic treatment should be as follows: The main target should be a MAP ⬎ 70 mm Hg to provide safe organ perfusion, particularly to the kidneys. If the MAP ⬍ 70 mm Hg, a volume challenge up to a CVP of 10 mm Hg, or if a Swan-Ganz catheter is available, to a PCWP of 15 mm Hg must be applied. If there is no success and the MAP maintained ⬍ 70 mm Hg, a vasopressor like norepinephrine must be administered. The volume and catecholamine
SANER
treatment have to be adjusted according to the data obtained by the Swan-Ganz catheter. As an alternative, a Picco system can be used. In septic patients Briegel et al17 showed that the use of supraphysiologic doses of hydrocortisone significantly reduced the necessity for vasopressor treatment. According to these data the use of hydrocortisone may lower the dose of vasopressor. Beside the blood loss, risk factors on the patient side that can facilitate PRLF must be considered: small remnant liver volume,18 advanced age,19 steatosis and cirrhosis,19,20 and preoperative chemotherapy.21 Patients with a healthy liver will survive a 75% resection.18,22 However, there is a wide individual range. The microcirculation is impaired among patients displaying steatosis or even cirrhosis. These livers are less resistant to ischemia-reperfusion injury, showing more mitochondrial dysfunction.23 Moreover, patients with cirrhosis show remarkably impaired hepatocyte regeneration.24 Preoperative chemotherapy can shrink a nonresectable tumor in 15% of cases to a resectable status.25 However, chemotherapy may also harm the liver, facilitating PRLF. Oxaliplatin may induce a veno-occlusive syndrome,26 which may be amplified after liver resetion, inducing Budd-Chiari syndrome. Irinotecan may lead to chemotherapy-associated steatohepatitis (CASH).27 Although many liver function tests are available indocyanin green disappearance rate (ICGDIS), aminopyrine breath test, MEGX test, and galactose elimination—the data reported in the literature are conflicting.28,29 Renal failure following liver resection can be caused by acute tubular necrosis or by development of hepatorenal syndrome. If the MAP drops below 80 mm Hg, the GFR will significantly decrease,4 causing activation of the vasoconstrictor systems—renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS). The vasoconstriction of the vas afferens lowers the GFR, causing necrosis and apoptosis of tubular cells, which are sloughed obstructing the lumen. The ultrafiltrate is resorbed by backleak from the peritubular vessels with complete deterioration of the GFR13 (Fig 2). The pathophysiologic changes in hepatorenal syndrome consist of intravascular hypovolemia with activation of the RAAS and SNS vasoconstrictor systems, leading to vasoconstriction of the vas afferens and subsequent decrease in the GFR. Initially there are no histological changes in the kidneys. If the liver function is improved, the kidneys recover.30 There are no reliable treatments for PRLF. Extracorporeal detoxification systems like MARS or Prometheus may be helpful, as already published for acute-on-chronic end-stage liver disease patients.31,32 There is only a single publication considering MARS for postoperative liver failure. The authors described 5 patients suffering from PRLF who were unsuccessfully treated with MARS. All patients died.33 There are no data concerning Prometheus and PRLF. Plasma separation (PS) can also be used as a rescue treatment. PS provides more hemodynamic stability and improves hepatic encephalopathy.34 We have treated 14
KIDNEY FAILURE FOLLOWING LIVER RESECTION
1223
Fig 2. (A–C) Vasoconstriction of the vas afferens lowers the GFR.
PRLF patients with PS, all of whom suffered from acute lung injury (ALI: Horovitz index ⬍ 300 mm Hg), needed high-dose noradrenaline support (⬎0.5 g/kg/min), and had acute renal failure with requirements for RRT. Eight of these 14 patients were cured and discharged in good clinical condition after an extended hospital stay. In conclusion, patients following liver resection require stable hemodynamics to avoid kidney failure. A precondition is an euvolemic patient with a CVP between 5 to 10 mm Hg. We need better patient selection to prevent renal failure. Extracorporeal detoxification systems are available, but show only limited effects.
REFERENCES 1. Belghiti J, Hiramatsu K, Benoist S, et al: Seven hundred forty-seven hepatectomies in the 1990s: an update to evaluate the actual risk of liver resection. J Am Coll Surg 191:38, 2000 2. Poon RT, Fan ST, Lo CM, et al: Improving perioperative outcome expands the role of hepatectomy in management of benign and malignant hepatobiliary diseases: analysis of 1222 consecutive patients from a prospective database. Ann Surg 240: 698, 2004 3. Jarnagin WR, Gonen M, Fong Y, et al: Improvement in perioperative outcome after hepatic resection: analysis of 1,803 consecutive cases over the past decade. Ann Surg 236:397, 2002 4. Thadhani R, Pascual M, Bonventre JV: Acute renal failure. N Engl J Med 334:1448, 1996 5. Imamura H, Seyama Y, Kokudo N, et al: One thousand fifty-six hepatectomies without mortality in 8 years. Arch Surg 138:1198, 2003 6. Kooby DA, Stockman J, Ben-Porat L, et al: Influence of transfusions on perioperative and long-term outcome in patients following hepatic resection for colorectal metastases. Ann Surg 237:860, 2003 7. Jones RM, Moulton CE, Hardy KJ: Central venous pressure and its effect on blood loss during liver resection. Br J Surg 85:1058, 1998 8. Melendez JA, Arslan V, Fischer ME, et al: Perioperative outcomes of major hepatic resections under low central venous pressure anesthesia: blood loss, blood transfusion, and the risk of postoperative renal dysfunction. J Am Coll Surg 187:620, 1998 9. McGilvray ID, Greig PD: Critical care of the liver transplant patient: an update. Curr Opin Crit Care 8:178, 2002 10. Kowalski HJ, Abelmann WH: The cardiac output in Laennec’s cirrhosis. J Clin Invest 32:1025, 1953 11. Pizcueta P, Pique JM, Fernandez M, et al: Modulation of the hyperdynamic circulation of cirrhotic rats by nitric oxide inhibition. Gastroenterology 103:1909, 1992
12. Albillos A, Rossi I, Cacho G, et al: Enhanced endotheliumdependent vasodilation in patients with cirrhosis. Am J Physiol 268:G459, 1995 13. Abuelo JG: Normotensive ischemic acute renal failure. N Engl J Med 357:797, 2007 14. Chhibber A, Dziak J, Kolano J, et al: Anesthesia care for adult live donor hepatectomy: our experiences with 100 cases. Liver Transpl 13:537, 2007 15. Schroeder RA, Collins BH, Tuttle-Newhall E, et al: Intraoperative fluid management during orthotopic liver transplantation. J Cardiothorac Vasc Anesth 18:438, 2004 16. Saner FH, Pavlakovic G, Gu Y, et al: Does PEEP impair the hepatic outflow in patients following liver transplantation? Intensive Care Med 32:1584, 2006 17. Briegel J, Forst H, Haller M, et al: Stress doses of hydrocortisone reverse hyperdynamic septic shock: a prospective, randomized, double-blind, single-center study. Crit Care Med 27:723, 1999 18. Schindl MJ, Redhead DN, Fearon KC, et al: The value of residual liver volume as a predictor of hepatic dysfunction and infection after major liver resection. Gut 54:289, 2005 19. Balzan S, Belghiti J, Farges O, et al: The “50 –50 criteria” on postoperative day 5: an accurate predictor of liver failure and death after hepatectomy. Ann Surg 242:824, 2005 20. Shirabe K, Shimada M, Gion T, et al: Postoperative liver failure after major hepatic resection for hepatocellular carcinoma in the modern era with special reference to remnant liver volume. J Am Coll Surg 188:304, 1999 21. Fong Y, Bentrem DJ: CASH (chemotherapy-associated steatohepatitis) costs. Ann Surg 243:8, 2006 22. Shoup M, Gonen M, D’Angelica M, et al: Volumetric analysis predicts hepatic dysfunction in patients undergoing major liver resection. J Gastrointest Surg 7:325, 2003 23. Seifalian AM, Piasecki C, Agarwal A, et al: The effect of graded steatosis on flow in the hepatic parenchymal microcirculation. Transplantation 68:780, 1999 24. Yamanaka N, Okamoto E, Kawamura E, et al: Dynamics of normal and injured human liver regeneration after hepatectomy as assessed on the basis of computed tomography and liver function. Hepatology 18:79, 1993 25. Adam R, Huguet E, Azoulay D, et al: Hepatic resection after down-staging of unresectable hepatic colorectal metastases. Surg Oncol Clin N Am 12:211, 2003 26. Rubbia-Brandt L, Mentha G, Terris B: Sinusoidal obstruction syndrome is a major feature of hepatic lesions associated with oxaliplatin neoadjuvant chemotherapy for liver colorectal metastases. J Am Coll Surg 202:199, 2006 27. Morris-Stiff G, Tan YM, Vauthey JN: Hepatic complications following preoperative chemotherapy with oxaliplatin or irinotecan for hepatic colorectal metastases. Eur J Surg Oncol 2007
1224 28. Gazzaniga GM, Cappato S, Belli FE, et al: Assessment of hepatic reserve for the indication of hepatic resection: how I do it. J Hepatobiliary Pancreat Surg 12:27, 2005 29. Lau H, Man K, Fan ST, et al: Evaluation of preoperative hepatic function in patients with hepatocellular carcinoma undergoing hepatectomy. Br J Surg 84:1255, 1997 30. Gines P, Guevara M, Arroyo V, et al: Hepatorenal syndrome. Lancet 362:1819, 2003 31. Heemann U, Treichel U, Loock J, et al: Albumin dialysis in cirrhosis with superimposed acute liver injury: a prospective, controlled study. Hepatology 36:949, 2002
SANER 32. Stange J, Mitzner SR, Klammt S, et al: Liver support by extracorporeal blood purification: a clinical observation. Liver Transpl 6:603, 2000 33. Rittler P, Ketscher C, Inthorn D, et al: Use of the molecular adsorbent recycling system in the treatment of postoperative hepatic failure and septic multiple organ dysfunction—preliminary results. Liver Int 24:136, 2004 34. Saner F, Sotiropoulos GC, Radtke A, et al: Small-for-size syndrome after living-donor liver transplantation treated by “portal vein wrapping” and single plasmapheresis. Transplantation 79:625, 2005
L
IVER RESECTION is the only curative treatment for primary and metastatic liver tumors. Due to improved surgical techniques, as well as modern anesthesia and intensive care, this operation has become a routine procedure over the last 20 years with a reasonably low complication rate. Belghiti et al1 reported their experience in 747 liver resections with a mortality rate of 4.4%. These data were supported by another high-volume center located in Hong Kong. Poon et al2 published their experience in 1222 liver resections with a mortality rate of 4.5%. The SloanKettering Hospital (New York, NY, United States) reported a mortality of 3.1% among 1803 liver resections.3 In 2006 we recorded 322 patients following liver resections at our intensive care unit. The main diagnoses leading to liver resection were colorectal metastases (52%), followed by other metastases (20.1%) and hepatocellular carcinoma (HCC) with an incidence of 10.2%. Fifteen percent of all patients experienced a kidney injury, whereas about half of them (7.1% of all patients) required renal replacement therapy (RRT); 73% of patients who required RRT died. This observation showed the close relationship of acute renal failure in patients following liver resection, as already published in septic patients.4 There are 2 major risk factors for kidney failure in patients following liver resection: first, extensive blood loss during the operation, and second, postresectional liver failure (PRLF). Jarnagin et al3 and Imamura et al5 suggested that a blood loss of 1250 mL was a cutoff point for major complications like kidney injury. Kooby et al6 reported a significantly worse outcome even after 5 years, if the transfusion requirement exceeded 3 units of packed red cells (PRC). In the context of blood loss, the role of the central venous pressure (CVP) must be discussed: hepatobiliary surgeons rely on a low CVP (⬍5 mm Hg), as a CVP
⬎ 5 mm Hg may induce liver congestion with impaired liver outflow. Jones et al7 examined the impact of CVP on blood loss in liver resection. In this study, a CVP ⬎ 5 cm H20 (⫽ 3.75 mm Hg) induced a 5-fold greater blood loss compared with a CVP ⬍ 5 cm H20 (1000 vs 200 mL blood loss). Melendez8 from the Sloan-Kettering Hospital, New York, reported his experience in 496 liver resections whereas 38% were major liver resection (⬎ 3 segments). Guided by a special anesthesia protocol—fluid restriction, use of nitroglycerine, furosemide, systolic arterial pressure of 90 mm Hg was tolerated—the median blood loss was 645 mL. The rate of acute renal failure and RRT was only 3.1%. The hemodynamic changes in patients following liver resection are similar to those of patients with cirrhosis or acute liver failure (Fig 1).9 Depending on the remnant liver volume and on the quality of the liver (steatosis/cirrhosis), these problems will be evident. Kowalski and Abelmann10 reported in 1953 that cardiac output (CO) in cirrhotic patients was significantly higher compared with healthy volunteers. The reason for this so-called hyperdynamic state is the huge concentration of nitric oxide (NO) in the circulation, as shown in both animal11 and clinical12 trials. As a result, the cGMP concentration is increased in the splanchnic area with severe vasodilation, declining central and arterial blood volume, low pulmonary capillary wedge pressure (PCWP), low CVP, low systemic vascular resistance (SVR), increased CO, and reduced mean arterial pressure (MAP). From the Universitätsklinikum Essen, Klinik für Allgemein-, Viszeral- und Transplantationschirurgie, Essen, Germany. Address reprint requests to F. Saner, MD, Universitätsklinikum Essen, Klinik für Allgemein-, Viszeral- und Transplantationschirurgie, Hufelandstr. 55, 45 122 Essen, Germany. E-mail: fuat.saner@ uni-due.de
© 2008 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710
0041-1345/08/$–see front matter doi:10.1016/j.transproceed.2008.03.068
Transplantation Proceedings, 40, 1221–1224 (2008)
1221
1222
Fig 1. Due to increased translocation of bacteria and an impaired phagocytosis activity of the Kupffer cells in patients with liver failure an increased cytokine production is evident. Inducible nitric oxide synthase (iNOS) activity will be increased with huge amounts of nitric oxide. As a result, the cGMP concentration is increased in the splanchnic area with severe vasodilation, declining central and arterial blood volume, low pulmonary capillary wedge pressure (PCWP), low central venous pressure (CVP), low systemic vascular resistance (SVR), and increased cardiac output (CO).
The kidneys are most at risk from a pressure drop. They can maintain their blood flow in the MAP range between 80 and 120 mm Hg. If the MAP falls to ⬍80 mm Hg, there is a significant drop in the glomerular filtration rate (GFR).13 Recently, the role of CVP and blood loss has been challenged. Chhibber et al14 described no correlation between CVP and blood loss among 100 live liver donors. In a retrospective study, Schroeder et al15 compared 2 CVP policies: a low CVP group (median 3 mm Hg) and a high CVP group (median 8 mm Hg). They confirmed the data of Jones et al7 that a higher CVP induced more blood loss. However, in the low CVP group the rate of kidney injury, the requirement for dialysis, and the 30-day mortality rate were significantly higher compared with the high CVP group. Another study16 reported the effects of 3 different CVP levels on the flow velocities of the hepatic artery (HA), the portal vein (PV), and the hepatic vein (HV) in liver transplant patients. Three CVP levels (6, 8, or 9 mm Hg) were applied to the patients. There were no significant changes in flow velocities of all 3 vessels. Based on these data, the hemodynamic treatment should be as follows: The main target should be a MAP ⬎ 70 mm Hg to provide safe organ perfusion, particularly to the kidneys. If the MAP ⬍ 70 mm Hg, a volume challenge up to a CVP of 10 mm Hg, or if a Swan-Ganz catheter is available, to a PCWP of 15 mm Hg must be applied. If there is no success and the MAP maintained ⬍ 70 mm Hg, a vasopressor like norepinephrine must be administered. The volume and catecholamine
SANER
treatment have to be adjusted according to the data obtained by the Swan-Ganz catheter. As an alternative, a Picco system can be used. In septic patients Briegel et al17 showed that the use of supraphysiologic doses of hydrocortisone significantly reduced the necessity for vasopressor treatment. According to these data the use of hydrocortisone may lower the dose of vasopressor. Beside the blood loss, risk factors on the patient side that can facilitate PRLF must be considered: small remnant liver volume,18 advanced age,19 steatosis and cirrhosis,19,20 and preoperative chemotherapy.21 Patients with a healthy liver will survive a 75% resection.18,22 However, there is a wide individual range. The microcirculation is impaired among patients displaying steatosis or even cirrhosis. These livers are less resistant to ischemia-reperfusion injury, showing more mitochondrial dysfunction.23 Moreover, patients with cirrhosis show remarkably impaired hepatocyte regeneration.24 Preoperative chemotherapy can shrink a nonresectable tumor in 15% of cases to a resectable status.25 However, chemotherapy may also harm the liver, facilitating PRLF. Oxaliplatin may induce a veno-occlusive syndrome,26 which may be amplified after liver resetion, inducing Budd-Chiari syndrome. Irinotecan may lead to chemotherapy-associated steatohepatitis (CASH).27 Although many liver function tests are available indocyanin green disappearance rate (ICGDIS), aminopyrine breath test, MEGX test, and galactose elimination—the data reported in the literature are conflicting.28,29 Renal failure following liver resection can be caused by acute tubular necrosis or by development of hepatorenal syndrome. If the MAP drops below 80 mm Hg, the GFR will significantly decrease,4 causing activation of the vasoconstrictor systems—renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS). The vasoconstriction of the vas afferens lowers the GFR, causing necrosis and apoptosis of tubular cells, which are sloughed obstructing the lumen. The ultrafiltrate is resorbed by backleak from the peritubular vessels with complete deterioration of the GFR13 (Fig 2). The pathophysiologic changes in hepatorenal syndrome consist of intravascular hypovolemia with activation of the RAAS and SNS vasoconstrictor systems, leading to vasoconstriction of the vas afferens and subsequent decrease in the GFR. Initially there are no histological changes in the kidneys. If the liver function is improved, the kidneys recover.30 There are no reliable treatments for PRLF. Extracorporeal detoxification systems like MARS or Prometheus may be helpful, as already published for acute-on-chronic end-stage liver disease patients.31,32 There is only a single publication considering MARS for postoperative liver failure. The authors described 5 patients suffering from PRLF who were unsuccessfully treated with MARS. All patients died.33 There are no data concerning Prometheus and PRLF. Plasma separation (PS) can also be used as a rescue treatment. PS provides more hemodynamic stability and improves hepatic encephalopathy.34 We have treated 14
KIDNEY FAILURE FOLLOWING LIVER RESECTION
1223
Fig 2. (A–C) Vasoconstriction of the vas afferens lowers the GFR.
PRLF patients with PS, all of whom suffered from acute lung injury (ALI: Horovitz index ⬍ 300 mm Hg), needed high-dose noradrenaline support (⬎0.5 g/kg/min), and had acute renal failure with requirements for RRT. Eight of these 14 patients were cured and discharged in good clinical condition after an extended hospital stay. In conclusion, patients following liver resection require stable hemodynamics to avoid kidney failure. A precondition is an euvolemic patient with a CVP between 5 to 10 mm Hg. We need better patient selection to prevent renal failure. Extracorporeal detoxification systems are available, but show only limited effects.
REFERENCES 1. Belghiti J, Hiramatsu K, Benoist S, et al: Seven hundred forty-seven hepatectomies in the 1990s: an update to evaluate the actual risk of liver resection. J Am Coll Surg 191:38, 2000 2. Poon RT, Fan ST, Lo CM, et al: Improving perioperative outcome expands the role of hepatectomy in management of benign and malignant hepatobiliary diseases: analysis of 1222 consecutive patients from a prospective database. Ann Surg 240: 698, 2004 3. Jarnagin WR, Gonen M, Fong Y, et al: Improvement in perioperative outcome after hepatic resection: analysis of 1,803 consecutive cases over the past decade. Ann Surg 236:397, 2002 4. Thadhani R, Pascual M, Bonventre JV: Acute renal failure. N Engl J Med 334:1448, 1996 5. Imamura H, Seyama Y, Kokudo N, et al: One thousand fifty-six hepatectomies without mortality in 8 years. Arch Surg 138:1198, 2003 6. Kooby DA, Stockman J, Ben-Porat L, et al: Influence of transfusions on perioperative and long-term outcome in patients following hepatic resection for colorectal metastases. Ann Surg 237:860, 2003 7. Jones RM, Moulton CE, Hardy KJ: Central venous pressure and its effect on blood loss during liver resection. Br J Surg 85:1058, 1998 8. Melendez JA, Arslan V, Fischer ME, et al: Perioperative outcomes of major hepatic resections under low central venous pressure anesthesia: blood loss, blood transfusion, and the risk of postoperative renal dysfunction. J Am Coll Surg 187:620, 1998 9. McGilvray ID, Greig PD: Critical care of the liver transplant patient: an update. Curr Opin Crit Care 8:178, 2002 10. Kowalski HJ, Abelmann WH: The cardiac output in Laennec’s cirrhosis. J Clin Invest 32:1025, 1953 11. Pizcueta P, Pique JM, Fernandez M, et al: Modulation of the hyperdynamic circulation of cirrhotic rats by nitric oxide inhibition. Gastroenterology 103:1909, 1992
12. Albillos A, Rossi I, Cacho G, et al: Enhanced endotheliumdependent vasodilation in patients with cirrhosis. Am J Physiol 268:G459, 1995 13. Abuelo JG: Normotensive ischemic acute renal failure. N Engl J Med 357:797, 2007 14. Chhibber A, Dziak J, Kolano J, et al: Anesthesia care for adult live donor hepatectomy: our experiences with 100 cases. Liver Transpl 13:537, 2007 15. Schroeder RA, Collins BH, Tuttle-Newhall E, et al: Intraoperative fluid management during orthotopic liver transplantation. J Cardiothorac Vasc Anesth 18:438, 2004 16. Saner FH, Pavlakovic G, Gu Y, et al: Does PEEP impair the hepatic outflow in patients following liver transplantation? Intensive Care Med 32:1584, 2006 17. Briegel J, Forst H, Haller M, et al: Stress doses of hydrocortisone reverse hyperdynamic septic shock: a prospective, randomized, double-blind, single-center study. Crit Care Med 27:723, 1999 18. Schindl MJ, Redhead DN, Fearon KC, et al: The value of residual liver volume as a predictor of hepatic dysfunction and infection after major liver resection. Gut 54:289, 2005 19. Balzan S, Belghiti J, Farges O, et al: The “50 –50 criteria” on postoperative day 5: an accurate predictor of liver failure and death after hepatectomy. Ann Surg 242:824, 2005 20. Shirabe K, Shimada M, Gion T, et al: Postoperative liver failure after major hepatic resection for hepatocellular carcinoma in the modern era with special reference to remnant liver volume. J Am Coll Surg 188:304, 1999 21. Fong Y, Bentrem DJ: CASH (chemotherapy-associated steatohepatitis) costs. Ann Surg 243:8, 2006 22. Shoup M, Gonen M, D’Angelica M, et al: Volumetric analysis predicts hepatic dysfunction in patients undergoing major liver resection. J Gastrointest Surg 7:325, 2003 23. Seifalian AM, Piasecki C, Agarwal A, et al: The effect of graded steatosis on flow in the hepatic parenchymal microcirculation. Transplantation 68:780, 1999 24. Yamanaka N, Okamoto E, Kawamura E, et al: Dynamics of normal and injured human liver regeneration after hepatectomy as assessed on the basis of computed tomography and liver function. Hepatology 18:79, 1993 25. Adam R, Huguet E, Azoulay D, et al: Hepatic resection after down-staging of unresectable hepatic colorectal metastases. Surg Oncol Clin N Am 12:211, 2003 26. Rubbia-Brandt L, Mentha G, Terris B: Sinusoidal obstruction syndrome is a major feature of hepatic lesions associated with oxaliplatin neoadjuvant chemotherapy for liver colorectal metastases. J Am Coll Surg 202:199, 2006 27. Morris-Stiff G, Tan YM, Vauthey JN: Hepatic complications following preoperative chemotherapy with oxaliplatin or irinotecan for hepatic colorectal metastases. Eur J Surg Oncol 2007
1224 28. Gazzaniga GM, Cappato S, Belli FE, et al: Assessment of hepatic reserve for the indication of hepatic resection: how I do it. J Hepatobiliary Pancreat Surg 12:27, 2005 29. Lau H, Man K, Fan ST, et al: Evaluation of preoperative hepatic function in patients with hepatocellular carcinoma undergoing hepatectomy. Br J Surg 84:1255, 1997 30. Gines P, Guevara M, Arroyo V, et al: Hepatorenal syndrome. Lancet 362:1819, 2003 31. Heemann U, Treichel U, Loock J, et al: Albumin dialysis in cirrhosis with superimposed acute liver injury: a prospective, controlled study. Hepatology 36:949, 2002
SANER 32. Stange J, Mitzner SR, Klammt S, et al: Liver support by extracorporeal blood purification: a clinical observation. Liver Transpl 6:603, 2000 33. Rittler P, Ketscher C, Inthorn D, et al: Use of the molecular adsorbent recycling system in the treatment of postoperative hepatic failure and septic multiple organ dysfunction—preliminary results. Liver Int 24:136, 2004 34. Saner F, Sotiropoulos GC, Radtke A, et al: Small-for-size syndrome after living-donor liver transplantation treated by “portal vein wrapping” and single plasmapheresis. Transplantation 79:625, 2005