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J Thorac Cardiovasc Surg 1994;108:700-708
© 1994 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

Monitoring of hepatic venous oxygen saturation for predicting acute liver dysfunction after Fontan operations

Osaka, Japan

From the Department of Surgery and Intensive Care Unit, Osaka University Medical School, Suita, Osaka, Japan.

Received for publication Nov. 2, 1993. Accepted for publication April 7, 1994. Address for reprints: Hikaru Matsuda, MD, 2-2 Yamadaoka, Suita, Osaka, 565, Japan.

Abstract

Acute liver dysfunction after Fontan operations may result from inadequate hepatic perfusion along with low cardiac output and high central venous pressure. We monitored hepatic venous oxygen saturation in 15 patients after Fontan operations to determine whether oxygen saturation predicts the occurrence and severity of acute liver dysfunction. We measured oxygen saturation from hepatic venous blood samples every 4 to 5 hours for at least 24 hours after the operation and used the mean hepatic venous oxygen saturation value for the first 24 hours after the operation to analyze the relationship between oxygen saturation and hepatic function. As indices of hepatic function, we measured serum alanine aminotransferase, total bilirubin, blood lactate (arterial, hepatic venous, and the difference between them), and the arterial ketone body ratio (the ratio of aceto-acetate to ß-hydroxybutyrate). For alanine aminotransferase and bilirubin, we used the maximal values during the first week in the analysis, and for blood lactate and ketone body ratio, we used the mean values for the first 24 hours after the operation. Significant broken-line regression relationships existed between mean hepatic venous oxygen saturation and hepatic function indices (alanine aminotransferase, total bilirubin, and blood lactate). The interpretation of these relationships is that hepatic indices are constant above the critical mean hepatic venous oxygen saturation values but are correlated with mean hepatic venous oxygen saturation below critical points in the range of 21% to 26%. Thus a hepatic venous oxygen saturation value below about 25% during the first 24 hours after a Fontan operation predicts the occurrence and the severity of acute liver dysfunction. We suggest that monitoring hepatic venous oxygen saturation is useful for management of critically ill patients after Fontan operations. (J THORACCARDIOVASCSURG1994;108:700-8)

Acute liver dysfunction, characterized by sharp increases in concentrations of serum transaminase and bilirubin, though infrequent, is a major complication after cardiac surgery. ^1,2 This complication is particularly likely to develop in patients who undergo Fontan operations, which bypass the right ventricle. After this type of operation, cardiac output is likely to be low and central venous pressure high. These altered hemodynamics may decrease blood flow to the liver, thus causing hypoxia in hepatic tissue, which in turn damages hepatic cells and ultimately manifests as acute liver dysfunction. ^3,4 In addition, coagulation system disorders resulting in bleeding tendency ³ or venous thrombosis ⁵ have also been reported as an early complication of Fontan operations. Therefore it is important to prevent liver dysfunction.

For this purpose, it is necessary to be able to predict the occurrence and severity of acute liver dysfunction. Prediction based on hemodynamic variables is complicated because many hemodynamic variables may interact with each other and thus affect hepatic perfusion. ^4,6,7 A more reliable prediction might be based on hepatic perfusion status, which can be assessed by measuring hepatic venous oxygen saturation (ShvO₂), as a reflection of oxygen supply-demand relationship. ^8,9 This predictor was suggested by our observation that ShvO₂ was extremely low in three patients who had acute liver dysfunction after Fontan operations. ⁴ We here report that monitoring ShvO₂ predicts the occurrence and the severity of acute liver dysfunction in patients after Fontan operations.

PATIENTS AND METHODS

Patients
Fifteen consecutive patients who underwent a modified Fontan operation were studied. Their ages ranged from 3 to 20 years (6.9 ± 4.7, mean ± standard deviation). Major cardiac anomalies were single right ventricle in six patients, single left ventricle in two patients, tricuspid atresia in three patients, mitral atresia in two patients, and pulmonary atresia with intact ventricular septum in two patients. Pulmonary vascular resistance before the operation ranged from 0.7 to 4.0 U · m² (1.9 ± 0.9 U · m²). No patient had evidence of hepatic dysfunction, as determined by routine biochemical testing. Operative procedures were atriopulmonary connection in eight patients and total cavopulmonary connection in the other seven patients. Anesthesia was maintained with fentanyl (0.05 to 0.1 mg/kg). Halothane was not used in these patients. Cardiopulmonary bypass was performed at moderate hypothermia (lowest blood temperature 24° to 28° C), and cardiopulmon ary bypass time ranged from 90 to 242 minutes. One patient died of septicemia and one of pulmonary venous obstruction on postoperative days 95 and 46, respectively. The other 13 patients were discharged without significant complications. The study was approved by the institutional human research committee, and informed consent was obtained from each patient's parents.

Technique of catheterizing the hepatic vein
After cardiopulmonary bypass, a curved metal stylet inside a sheath was inserted into the right hepatic vein through a small atriotomy secured with a pursestring suture at the junction of the right atrium and the inferior vena cava. It was easily confirmed that the stylet was in the right hepatic vein because the right hepatic vein advanced toward the right, away from the inferior vena cava. The stylet was then withdrawn and a smaller catheter was advanced through the sheath. The catheter was advanced until it met resistance at the end of the hepatic vein; then it was withdrawn by about 2 cm to avoid wedging. The sheath was withdrawn and peeled off, with the catheter left in place. An additional elastic pursestring suture was placed around the site of insertion to prevent bleeding when the catheter was later withdrawn (Fig. 1). The other end of the catheter was brought outside transcutaneously. Proper position of the catheter was confirmed by postoperative radiograph in all patients. Usually, this catheter was removed on the second or third postoperative day before removal of the mediastinal drain.

View larger version (49K): [in this window] [in a new window]   Fig. 1. The method of placing a blood sampling catheter in the hepatic veinduring cardiac operation. A curved metal stylet inside a sheath is inserted into the right hepatic vein through a small atriotomy secured with a purse string suture (A). The stylet is withdrawn and a soft catheter is inserted through the sheath. The sheath is then withdrawn and peeled off the catheter (B). An additional purse string suture of elastic thread is placed around the site of insertion to prevent bleeding on withdrawal.

Hepatic function.
We measured two indices of hepatic cellular damage, serum alanine aminotransferase (ALT) and total bilirubin concentration, at least twice a day for at least 1 week after the operation.

In 13 patients, we measured blood lactate concentration (as an index of hepatic lactate metabolism) in arterial and hepatic venous blood at the same time as the blood oxygen saturation measurement. We also calculated the difference between arterial and hepatic venous lactate concentration.

In seven patients, we measured arterial ketone body ratio (as an index of hepatic mitochondrial oxidation-reduction [redox] state) at the same time as the blood oxygen saturation and lactate measurements. Arterial ketone body ratio was obtained as a ratio of aceto-acetate to ß-hydroxybutyrate. This ratio reflects hepatic mitochondrial nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide, reduced. ¹⁰ The patient's prognosis is poor when this ratio persistently drops below 0.4. ¹¹

ALT and bilirubin were measured spectrophotometrically by an automated analyzer (Hitachi type-736, Tokyo, Japan). Lactate and ketone bodies were measured enzymatically as described elsewhere. ^12-14 The enzymes for aceto-acetate and ß-hydroxybutyrate measurements were purchased from Sanwa Kagaku Co. Ltd. (Nagoya, Japan) and other enzymes from Boehringer Mannheim GmbH (Mannheim, Germany).

Hemodynamics.
Mean arterial pressure and central venous pressure (CVP) were monitored continuously. Cardiac index was measured at least twice during the first 24 hours after the operation by the dye-dilution method (injection into the left atrium and detection in the radial artery) in 11 patients.

Postoperative management
Inotropic support (dopamine, dobutamine, or isoproterenol) and a vasodilator (prostaglandin E₁) were used in most patients. Postoperative management was based primarily on hemodynamic variables, and all efforts were made to improve the hemodynamic variables when they deteriorated.

Data analysis
The relationship between ShvO₂ and hepatic function.
For ShvO₂, we computed the mean values during the first 24 hours after the operation and used them in the analysis of the relationship between ShvO₂ and hepatic function. We denoted these values with the prefix mean. The reason we used the mean ShvO₂ value for the first 24 hours after the operation is that ischemic hepatitis (severe hepatic dysfunction that occurs after circulatory shock) has been reported to develop when shock lasts for 24 hours. ¹⁵ In assessing the hepatic function indices, we used two different types of values. For ALT and total bilirubin, we used maximal values during the first operative week and denoted them with the prefix max. For lactate concentration and arterial ketone body ratio, we computed the mean values as described earlier and used them in the analysis. The reason we distinguished these values as max and mean is that ALT and total bilirubin change rather slowly, whereas blood lactate and ketone body ratio change quickly along with the hepatic condition.

Because oxygen consumption remains relatively constant above the critical oxygen delivery level, and decreases in proportion to the decrease in oxygen delivery below the critical delivery level, ^8,16,17 we analyzed the relationshipbetween ShvO₂ and hepatic function with the broken-line regression ¹⁸:

where Y = the hepatic function index, y_i = independent (constant) value for the hepatic function index where X > x_c, s = slope of the regression line where X x_c, X = ShvO₂, and x_c = the critical value in ShvO₂ where the line bends (Fig. 2). In this relationship, above the critical ShvO₂ level x_c, hepatic function is independent of ShvO₂. However, below x_c hepatic function linearly depends on ShvO₂ with a slope of s. The parameters y_i, s, and x_c were estimated by nonlinear least squares with the Marquard-Levennberg algorithm. ¹⁹

View larger version (14K): [in this window] [in a new window]   Fig. 2. Broken-line relationship between hepatic venous oxygen saturation (ShvO2) and hepatic function. The hepatic function index remains at yi independent of ShvO2 above the critical ShvO2 level (xc) but is correlated with ShvO2 with a slope (s) below the critical level (xc).

Statistical analysis.
Data are summarized as mean ± standard deviation for basic statistics. In the broken-line regression analysis, each parameter is reported as the estimate ± the standard error of the estimate, and the associated t statistic was tested for statistical significance.

Statistical analysis was done with SigmaStat Release 1.02 (Jandel Scientific, San Rafael, Calif.). Statistical significance was based on a p value less than 0.05.

RESULTS

Postoperative course of a patient with acute liver dysfunction
A typical postoperative course of a patient in whom acute liver dysfunction developed is shown in Fig. 3. In this patient, the CVP rose to 20 to 25 mm Hg early after the operation. Cardiac output remained in the relatively low range of 2.0 to 2.4 L/min/per square meter on the first operative day. ShvO₂ was low (below 10%) immediately after the operation. It rose to 20% on the second postoperative day and to 30% to 40% on the third day. Simultaneously measured superior vena caval oxygen saturation ranged from 55% to 70%. ALT concentration started increasing about 24 hours after the operation, reaching the maximum value of 4050 U/L on the third postoperative day. Total bilirubin concentration started increasing slightly later than the ALT did, reaching 7.3 mg/dl on the sixth postoperative day. It took more than 1 month for total bilirubin to return to normal.

View larger version (23K): [in this window] [in a new window]   Fig. 3. Postoperative change in venous oxygen saturations, hemodynamics, and hepatic function in a patient who had acute liver dysfunction after a Fontan operation. ShvO2, Hepatic venous oxygen saturation; SvO2, superior vena caval oxygen saturation; CI, cardiac index; CVP, central venous pressure; ALT, serum alanine aminotransferase; TB, serum total bilirubin.

View larger version (27K): [in this window] [in a new window]   Fig. 4. Relationship between mean ShvO2 and postoperative hepatic function. ShvO2, Hepatic venous oxygen saturation; ALT, alanine aminotransferase; TB, total bilirubin; La, arterial lactate; Lhv, hepatic venous lactate; La-hv, difference between arterial and hepatic venous lactate; AKBR, arterial ketone body ratio; mean, mean value during the first 24 hours after the operation; max, maximal value during the first week after the operation.

DISCUSSION

We here report that a mean ShvO₂ value of less than about 25% for the first 24 hours after a Fontan operation predicts the occurrence and severity of acute liver dysfunction. In our 15 patients, we found that when ShvO₂ was less than about 25%, transaminase and bilirubin concentrations were increased, indicating cell damage, and blood lactate was increased, indicating impaired hepatic lactate metabolism. Furthermore, the lower the ShvO₂, the more severe the liver dysfunction. For example, in a patient whose mean ShvO₂ was 10%, hepatic function indices had extremely high values: max ALT was 4050 U/L, max total bilirubin 7.3 mg/dl, and mean arterial lactate 93 mg/dl.

Our findings are consistent with those from animal studies, which showed that hepatic functions, such as hepatic lactate uptake, ²² hepatic oxygen uptake, ^8,23 hepatic ethanol uptake, and bile flow ²⁴ are impaired when hepatic venous oxygen tension decreases below a range of 5 to 28 mm Hg.

The main advantage of using ShvO₂ to predict acute liver dysfunction is its speed. The standard hepatic function indices, serum enzymes or bilirubin take 24 to 48 hours to increase after the operation. By then, it may be too late to treat these patients successfully. In contrast, ShvO₂ clearly detects signs of acute liver dysfunction even during the operation. Treatment can begin immediately and thus has a better chance of success.

Monitoring and treatment were successful in the patients in this study. We monitored ShvO₂ continuously with a fiberoptic catheter in five patients and were able to assess the hepatic oxygen supply-demand relationship in real time. Treatment was started during this monitoring even when other hemodynamic variables appeared acceptable, and acute liver dysfunction was prevented (Fig. 5). The optimal treatment is not yet established because the hemodynamic factors that affect ShvO₂ are multifactorial. Generally, the treatment is to increase catecholamines when left atrial pressure is high and to use volume loading and pulmonary vasodilation when left atrial pressure is low. However, volume loading may increase CVP and the increase may decrease hepatic blood flow. ^24-26 Therefore, careful assessment of the adequacy of the treatment by checking the response of ShvO₂ is mandatory.

View larger version (130K): [in this window] [in a new window]   Fig. 5. Continuous ShvO2 monitoring with a fiberoptic catheter. Immediately after the operation, ShvO2 showed markedly low values (below 20%). Even though the blood pressure seemed to be acceptable, the patient was treated by increasing catecholamines, which led to an increase in ShvO2. In this patient, liver dysfunction did not occur. ShvO2, Hepatic venous oxygen saturation; BP, arterial pressure; CVP, central venous pressure; ISP, isoproterenol; DOB, dobutamine; DOA, dopamine; PGE1, prostaglandin E1.

In this study, we found only a borderline correlation between ShvO₂ and hemodynamic variables. We ⁴ have previously reported that cardiac output may play a more significant role than CVP in causing acute liver dysfunction in patients after Fontan operations. We ⁹ have also shown, in dogs, that abdominal aortic flow contributes more significantly to ShvO₂ than inferior vena caval pressure does. From these results, we believe that cardiac output may play an important role in determining ShvO₂, although we could not clearly show it in this study. The lack of a significant correlation in the present study might have been due to the fact that we measured cardiac output in 11 of the 15 patients, and less frequently than other hemodynamic variables. Surprisingly, ShvO₂ was not correlated with superior vena caval oxygen saturation in this study, a finding that has previously been reported. ^27,28 This finding may indicate that the distribution of cardiac output to each organ changes in situations such as low cardiac output status or an unstable hemodynamic condition after cardiac surgery. Furthermore, inotropic drugs, which have been reported to alter hepatic blood flow, ^20,21 were not selected as significant variables relating to ShvO₂. Thus these drugs probably altered cardiac output or blood pressures but did not have an additional effect on hepatic blood flow in this study.

Some potential limitations of the study merit discussion. First, acute changes in hepatic function precipitated by injury to the liver may begin during rather than after the operation because of cannulation of the inferior vena cava, hypothermia, hypoperfusion, long duration of cardiopulmonary bypass, or other intraoperative factors. It is possible that these intraoperative factors might influence postoperative hepatic function directly (not through postoperative hepatic oxygen supply-demand status). However, this possibility seems unlikely because the patients in our study, who underwent relatively uniform operations and cardiopulmonary bypass procedures, had a variety of postoperative ShvO₂ values, and these values correlated significantly with hepatic function. Thus postoperative liver dysfunction in these patients must have been related to postoperative hepatic oxygen supply-demand status rather than to intraoperative factors. Second, although a correlation existed between ShvO₂ and early postoperative liver function, this correlation did not signal irreversible liver dysfunction. Most of the patients with low ShvO₂ recovered their normal hepatic function late after the operation. Thus one might think that changes in ShvO₂ poorly predict long-term liver dysfunction and that the importance of monitoring ShvO₂ should be minimized. However, although all our patients who had acute liver dysfunction recovered normal hepatic function, it took more than 1 month for their complete recovery. For example, serum total bilirubin 1 month after the operation was still twice as high in the six patients with an ShvO₂ less than 25% as in the nine patients with an ShvO₂ of 25% or more (1.9 ± 0.6 versus 0.8 ± 0.2 mg/dl, p < 0.001). Moreover, a significant correlation existed between the duration of intensive care unit stay and the mean ShvO₂ (r_s = - 0.75, p = 0.002) as assessed by Spearman rank correlation. Thus the morbidity of the patients with low ShvO₂ was greater than that of the patients with higher ShvO₂. Therefore we think that monitoring ShvO₂ for the prevention of acute liver dysfunction is a useful way to reduce the morbidity of the patients.

In summary, we here report that an ShvO₂ value below the critical point of about 25% for the first 24 hours after a Fontan operation predicts the occurrence and the severity of acute liver dysfunction. Although severe liver dysfunction is rare nowadays because of the use of newer modifications of the Fontan operation, in some patients operative risk is relatively high because of poor ventricular function or high pulmonary vascular resistance. Monitoring ShvO₂ may be useful for managing these critically ill patients after Fontan operations.

Acknowledgments

We thank Stanton A. Glantz, PhD, and Mimi Zeiger (University of California, San Francisco), for statistical advice and helpful comments on drafts of the manuscript, respectively, and Ryo Fushimi and Kikumi Hosotsubo (Osaka University Medical School) for assistance with the alanine aminotransferase, total bilirubin, and lactate measurements.

References

1. Mundth ED, Keller AR, Austen WG. Progressive hepatic and renal failure associated with low cardiac output following open-heart surgery. J THORAC CARDIOVASC SURG 1967;53:275-84.[Medline]
   
2. Hill DM, Warren SE, Mitas JA, Swerdlin AHR. Hepatic coma after open heart surgery. South Med J 1980;73:906-8.[Medline]
   
3. Jenkins JG, Lynn AM, Wood AE, Trusler GA, Barker GA. Acute hepatic failure following cardiac operation in children. J THORAC CARDIOVASC SURG 1982;84:865-71.[Abstract]
   
4. Matsuda H, Covino E, Hirose H, et al. Acute liver dysfunction after modified Fontan operation for complex cardiac lesions: analysis of contributing factors and its relation to the early prognosis. J THORAC CARDIOVASC SURG 1988;96:219-26.[Abstract]
   
5. Cromme-Dijkhuis AH, Henkens CM, Bijleveld CM, Hillege HL, Bom VJ, van der Meer J. Coagulation factor abnormalities as possible thrombotic risk factors after Fontan operations. Lancet 1990;336:1087-90.[Medline]
   
6. Nogaki H. Risk factors and management of deteriorated liver function following open-heart surgery in patients with pre-existing congestive liver dysfunction due to heart failure. Nippon Kyobu Geka Gakkai Zasshi 1984;32:1762-74.[Medline]
   
7. Onitsuka T, Koga Y, Shibata K, et al. The effects of hepatic perfusion pressure on hepatic insufficiency after open heart surgery for congenital heart disease. Nippon Kyoubu Geka Gakkai Zasshi 1986;34:336-42.
   
8. Nagano K, Gelman S, Parks DA, Bradley EL Jr. Hepatic oxygen supply-uptake relationship and metabolism during anesthesia in miniature pigs. Anesthesiology 1990;72:902-10.[Medline]
   
9. Takano H, Nakano S, Shirakura R, Kaneko M, Matsuda H. Experimental assessment of hepatic perfusion in circulatory failure: influence of low cardiac output and high venous pressure. Surg Forum 1991;42:216-8.
   
10. Williamson DH, Lund P, Krebs HA. The redox state of free nicotinamide-adenine dinucleotide in the cytoplasm and mitochondria of rat liver. Biochem J 1967;103:514-27.[Medline]
    
11. Ozawa K, Aoyama H, Yasuda K, et al. Metabolic abnormalities associated with postoperative organ failure: a redox theory. Arch Surg 1983;118:1245-51.[Abstract/Free Full Text]
    
12. Gutmann I, Wahlefeld AW. L-(+)–Lactate. In: Bergmeyer HU, ed. Methods of enzymatic analysis. New York: Academic Press, 1974:1464-8.
    
13. Mellanby J, Williamson DH. Acetoacetate. In: Bergmeyer HU, ed. Methods of enzymatic analysis. New York: Academic Press, 1974:1840-3.
    
14. Williamson DH, Mellanby J. D-(–)-3-Hydroxybutyrate. In: Bergmeyer HU, ed. Methods of enzymatic analysis. New York: Academic Press, 1974:1836-9.
    
15. Sherlock S. The liver in heart failure: relation of anatomical, functional and circulatory changes. Br Heart J 1951;13:273-93.
    
16. Lutz J, Henrich H, Bauereisen E. Oxygen supply and uptake in the liver and the intestine. Pflüegers Arch 1975;360:7-15.
    
17. Samsel RW, Cherqui D, Pietrabissa A, et al. Hepatic oxygen and lactate extraction during stagnant hypoxia. J Appl Physiol 1991;70:186-93.[Abstract/Free Full Text]
    
18. Samsel RW, Schumacker PT. Determination of the critical O₂ delivery from experimental data: sensitivity to error. J Appl Physiol 1988;64:2074-82.[Abstract/Free Full Text]
    
19. Glantz SA, Slinker BK. Nonlinear regression. In: Glantz SA, ed. The primer of applied regression and analysis of variance. New York: McGraw-Hill, 1990:482-94.
    
20. Bacq Y, Gaudin C, Hadengue A, et al. Systemic, splanchnic and renal hemodynamic effects of a dopaminergic dose of dopamine in patients with cirrhosis. Hepatology 1991;14:483-7.[Medline]
    
21. Kurokawa T, Nonami T, Harada A, et al. Effects of prostaglandin E₁ on the recovery of ischemia-induced liver mitochondrial dysfunction in rats with cirrhosis. Scand J Gastroenterol 1991;26:269-74.[Medline]
    
22. Tashkin DP, Goldstein PJ, Simmons DH. Hepatic lactate uptake during decreased liver perfusion and hypoxia. Am J Physiol 1972;223:968-74.[Free Full Text]
    
23. Larsen JA, Krarup N, Munck A. Liver hemodynamics and liver function in cats during graded hypoxic hypoxemia. Acta Physiol Scand 1976;98:257-62.[Medline]
    
24. Hanson KM, Johnson PC. Local control of hepatic arterial and portal venous flow in the dog. Am J Physiol 1966;211:712-20.[Free Full Text]
    
25. Lautt WW. Effects of acute, passive hepatic congestion on blood flow and oxygen uptake in the intact liver of the cat. Circ Res 1977;41:787-90.[Abstract/Free Full Text]
    
26. Hinshaw LB, Reins DA, Wittmers L. Venous-arteriolar response in the canine liver. Proc Soc Exp Biol Med 1965;118:979-82.
    
27. Kainuma M, Fujiwara Y, Kimura N, et al. Monitoring hepatic venous hemoglobin oxygen saturation in patients undergoing liver surgery. Anesthesiology 1991;74:49-52.[Medline]
    
28. Takano H, Matsuda H, Kaneko M, et al. Hepatic venous oxygen saturation monitoring in patients with assisted circulation for severe cardiac failure. Artif Organs 1991;15:248-52.[Medline]
    

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Hikaru Matsuda Yasuhisa Shimazaki Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Takano, H. Articles by Taenaka, N. Search for Related Content PubMed PubMed Citation Articles by Takano, H. Articles by Taenaka, N.