Abstract

To evaluate the haemodynamic effects of portal triad clamping (PTC) during laparoscopic liver resection, 10 patients without cardiac disease were studied by invasive monitoring including a pulmonary artery catheter and were compared with a control group of 10 patients undergoing liver resection by laparotomy. During laparoscopic surgery, intra‐abdominal pressure was kept below 14 mm Hg and minute ventilation was adjusted to prevent hypercapnia. Measurements were made before PTC (T1), 5 min after PTC (T2) and 5 min after clamp release (T3). During clamping with pneumoperitoneum, mean arterial pressure (MAP) remained stable (+2%; not significant), systemic vascular resistance (SVR) increased by 37% (P<0.01, T2 vs T1) and cardiac index (CI) decreased by 19% (P<0.01, T2 vs T1). During laparotomy and clamping, MAP increased by 18% (P<0.01, T2 vs T1), SVR increased by 36% (P<0.01, T2 vs T1) and CI decreased by 9% (not significant). We were unable to demonstrate a difference in haemodynamic changes during clamping with pneumoperitoneum vs the open surgical technique, but in a small number of patients this lack of difference could have been a result of inadequate statistical power. The haemodynamic changes that we found were well tolerated in these patients, who had normal cardiac function.

Br J Anaesth 2001; 87: 493–6

Accepted for publication: May 3, 2001

With greater experience in both laparoscopy and liver surgery, laparoscopy for some liver resections is now feasible and safe.1 During open abdominal liver surgery, portal triad clamping (PTC) can limit bleeding.2 Portal triad clamping typically increases mean arterial pressure (MAP) (+21%) and systemic vascular resistance (SVR) (+48%), and decreases cardiac output (–17%).3 Similar haemodynamic changes occur at the start of peritoneal insufflation.3 4 Some authors found the changes caused by pneumoperitoneum similar to those of chronic heart failure.5 As laparoscopic liver resection results in both types of change, potentially serious haemodynamic changes may occur.

We studied PTC performed during laparoscopy and compared the haemodynamic responses with the responses to PTC during laparotomy, and assessed the possible adverse effects of such changes.

Methods and results

After approval of the study by the investigational review board,1 patients were informed about the innovative nature of the procedure and their consent was obtained. Patients with left atrial dilation (>4.0 cm), left ventricular dilation (left ventricular end‐diastolic internal dimensions >5.7 cm), decreased shortening fraction (<31%), regional wall motion abnormalities, valvular heart disease, cardiomyopathy and pericardial disease were excluded from the study. We also excluded patients who had intraoperative bleeding, defined as the need for rapid volume expansion or blood transfusion before PTC, and patients with haemodynamic instability, defined as MAP variation greater than 10% before PTC.

Between May 1999 and February 2000, we studied 10 consecutive adult patients undergoing elective liver resection done laparoscopically (laparoscopy group). The liver segments that can be safely resected laparoscopically are the anterior and lateral segments (segments II–VI).1 Laparoscopic resection was performed for peripheral lesions 5 cm or less in size, and resections were limited to three segments or fewer.1 Tumours in posterior and superior segments (i.e. segments I, VII and VIII) should not be considered because of difficult laparoscopic access and connections with the inferior vena cava and major hepatic veins.1 The carbon dioxide pneumoperitoneum was induced with 14 mm Hg intra‐abdominal pressure in the supine position before a 20° head‐up tilt. A control group of 10 consecutive patients undergoing liver resection performed via an abdominal incision (open group) was studied similarly. Intermittent PTC was applied with 15‐min clamping and 5‐min release periods.6

Anaesthetic management and intraoperative care were standardized throughout the study. General anaesthesia was induced with thiopental 4–6 mg kg–1 and sufentanil 0.3 µg kg–1 i.v. After orotracheal intubation, facilitated with atracurium 0.5 mg kg–1, anaesthesia was maintained with 0.5–1.5% end‐tidal isoflurane together with a continuous infusion of sufentanil 0.3 µg kg–1 h–1, and muscular relaxation was maintained by a continuous infusion of atracurium 0.5 mg kg–1 h–1. Crystalloid solution was infused during operation at a basal rate of 10 ml kg–1 h–1. The inspired oxygen fraction was set at 50% in air and minute ventilation was adjusted to maintain arterial carbon dioxide below 45 mm Hg.

After induction of general anaesthesia, one radial artery was cannulated and a 7.5 F thermodilution Edwards Swan–Ganz catheter (Baxter, Irvine, CA, USA) was introduced via the right internal jugular vein. Pressures were obtained after calibration, zeroing to atmospheric pressure and using the midchest level as reference. We recorded MAP, pulmonary artery pressure, right atrial pressure and pulmonary artery occlusion pressure, all at end‐expiration. Cardiac output was measured using the thermodilution technique, and an extent of variation less than 10% was considered permissible when taking the average of three measurements.

The first period of PTC during the surgical procedure was studied. Haemodynamic data were collected 5 min before PTC (T1), 5 min after clamping (T2) and 5 min after clamp release (T3) in the two groups.

Data were analysed with the Statview 5.0 statistical packages (SAS Institute, Cary, NC, USA). Data are presented as mean (sd) unless otherwise stated. Intergroup comparisons were made with the χ2 test or Fisher’s exact test for categorical variables, and Student’s t‐test or the Mann–Whitney U‐test when appropriate for continuous variables. Changes in variables within the two groups were subjected to analysis of variance (ANOVA) followed by the Neuman–Keuls test, as appropriate. Assuming a decrease in CI of 30% to be clinically important, we estimated that 10 patients in each group would be adequate to test the null hypothesis at 0.05 significance with a power of 0.83. A P value <0.05 was considered statistically significant.

Study population

The two groups of patients were similar in clinical characteristics, duration of surgery before PTC, blood loss and total i.v. infusion (Table 1). No severe perioperative cardiopulmonary complications were observed. No vasoactive drugs were used during PTC. All patients recovered uneventfully, except for one patient who had nosocomial Legionnella pneumonia but recovered satisfactorily.

Haemodynamic values during PTC

At the time of data recording, body temperature was 34.8 (0.54)°C in the laparoscopy group and 35.1 (0.63)°C in the open group (not significant). Peak airway pressure was greater in the laparoscopy group [25 (4) vs 19 (2) cm H2O, P<0.003], as was Pco2, although this remained below 40 mm Hg. The pH value lay between 7.36 and 7.43 in both groups. The haemoglobin concentration was 11.6 (1.7) g dl–1 in the laparoscopy group and 12.5 (1.8) g dl–1 in open group (not significant), and remained stable throughout the PTC period.

Before PTC, haemodynamic values were similar in the two groups. In the laparoscopic procedures, during PTC, MAP remained stable [2 (11)%, not significant], SVR rose by 37 (45)% (T2 vs T1, P<0.01) and CI decreased by 19 (17)% (T2 vs T1, P<0.01) (Table 2). In the open procedures, during PTC, MAP increased by 18 (18)% (T2 vs T1, P<0.01), SVR increased by 36 (28)% (T2 vs T1, P<0.01) and CI decreased by 9 (16)% (not significant) (Table 2). There were no differences between the two groups other than a moderate increase in MAP in open group [open group, 108 (19) mm Hg; laparoscopy group, 84±8 mm Hg; P<0.05].

Comment

In our study, the haemodynamic changes associated with PTC during open procedures were less pronounced than those observed by Delvaet al.3 but were similar to those of a recent study.6 The anaesthetic technique could have affected these haemodynamic changes, as isoflurane was used in our study instead of enflurane in the study of Delvaet al.3 Dramatic haemodynamic changes after PTC during pneumoperitoneum have been reported in a pig model,7 with marked decreases in CI and MAP and an increase in heart rate.7 We found that the haemodynamic response was different in humans.

In the present study, conditions before PTC were similar in the two groups despite the pneumoperitoneum. Pneumoperitoneum causes increases in arterial pressure and SVR.4 Changes in cardiac output are variable, consistent with the Starling resistor concept of abdominal venous return.8 Moreover, the reverse Trendelenburg position causes a further decrease in preload.4 However, these haemodynamic changes were not sustained throughout the period of pneumoperitoneum.4 The partial correction of the haemodynamic variables during pneumoperitoneum may have been caused by the vasodilating properties of isoflurane.4

In fact, PTC during laparoscopy did not cause significant haemodynamic changes compared with the open procedures. The MAP was stable, CI decreased slightly and SVR increased. We suggest that an increase in SVR counteracted the moderate decrease in CI, so that MAP remained at the preclamping level. The mild decrease in CI could be explained by a preload that was insufficient38 to compensate for the increased stroke work necessary to maintain cardiac output.9 During the laparotomy, the normal heart could become sensitive to changes in afterload, as in heart failure.510 The mild decrease in CI during PTC performed under laparoscopy can be explained by a decrease in venous return and/or an increase in SVR. These haemodynamic changes were not great enough to necessitate stopping the procedure or to release the PTC.

In conclusion, in a small number of patients, we could not find a difference in haemodynamic changes during PTC during laparotomy, and PTC carried out during an open surgical procedure. However, this lack of difference could be a result of inadequate power of the study. Laparoscopic liver resections with PTC are feasible and safe in patients with normal cardiac function.

Acknowledgement

The authors thank Anne Labre (NA), Marie‐Christine Pollono (NA), René Choin (NA), and Frédéric Jean‐Claude (NA) for skilful technical help and assistance in the operating room.

Table 1

Patient characteristics. Unless otherwise stated, results are expressed as mean (sd) for continuous variables. P values are reported when <0.2, otherwise the difference is indicated as being not significant (NS)

Characteristic Laparoscopy group Open group P 
Age (yr) 58.1 (36–79) 65.6 (40–76) 0.2 
Sex (M/F) 7/3 8/2 NS 
Body surface area (m21.76 (0.22) 1.8 (0.20) NS 
Arterial hypertension (nNS 
Cirrhosis (nNS 
Pathological diagnoses (n   
 Primary liver cancer  
 Secondary liver cancer  
 Benign liver lesion 0.1 
Blood loss (ml) (median, 25th and 75th percentiles) 400 (275, 1000) 600 (400, 600) NS 
Total i.v. infusion (ml kg–143.4 (17.7) 36.9 (11.8) NS 
Transfusion (nNS 
Duration of surgery before PTC (min) 100 (44) 102 (48) NS 
Characteristic Laparoscopy group Open group P 
Age (yr) 58.1 (36–79) 65.6 (40–76) 0.2 
Sex (M/F) 7/3 8/2 NS 
Body surface area (m21.76 (0.22) 1.8 (0.20) NS 
Arterial hypertension (nNS 
Cirrhosis (nNS 
Pathological diagnoses (n   
 Primary liver cancer  
 Secondary liver cancer  
 Benign liver lesion 0.1 
Blood loss (ml) (median, 25th and 75th percentiles) 400 (275, 1000) 600 (400, 600) NS 
Total i.v. infusion (ml kg–143.4 (17.7) 36.9 (11.8) NS 
Transfusion (nNS 
Duration of surgery before PTC (min) 100 (44) 102 (48) NS 
Table 2

Comparisons of haemodynamic measurements in the laparoscopy (L) and open (O) groups before, during and after PTC. T1=5 min before portal triad clamping (PTC); T2=5 min after clamping; T3=5 min after clamp release. MAP=mean arterial pressure; HR=heart rate; RAP=right atrial pressure; PAOP=pulmonary artery occlusion pressure; MPAP=mean pulmonary artery pressure; CI=cardiac index; SVR=systemic vascular resistance; PVR=pulmonary vascular resistance. CI, SVR and PVR were calculated according to standard formulae. *Intergroup comparison, P<0.05. T2 vs T1=P<0.05 at T2 vs T1; T3 vs T2=P<0.05 at T3 vs T1. P values are reported when <0.2, otherwise the difference is indicated as being not significant (NS)

Variable T1 T2 T3 ANOVA results 
 Group L  Group O Group L Group O Group L Group O Group L Group O 
MAP (mm Hg) 84 (13) 92 (12) 84 (8) 108 (19)* 83 (8) 96 (13) NS  T2 vs T1 T3 vs T2 
HR (beats min–173 (12) 82 (14) 73 (11) 80 (15) 74 (10) 78 (13) NS  NS  
RAP (mm Hg) 9.0 (4.6) 7.6 (3.2) 7.4 (4.6) 6.0 (1.8) 9.5 (6.0) 6.6 (3.4) 0.12  0.13  
PAOP (mm Hg) 11.5 (4.7) 11.3 (2.0) 11.5 (5.5) 10.1 (2.0) 12.8 (5.2) 11.2 (3.4) NS  NS  
MPAP (mm Hg) 21 (6) 20 (2) 20 (5) 18 (3) 23 (7) 20 (5) T3 vs T2  NS  
CI (litre min–1 m–23.6 (1.5) 3.8 (1.2) 2.8 (1.3) 3.6 (1.9) 3.5 (1.1) 3.7 (1.1) T2 vs T1 T3 vs T2 NS  
SVR (dyne s cm–5 m–21846 (520) 1899 (596) 2480 (779) 2705 (1330) 1797 (489) 2062 (569) T2 vs T1 T3 vs T2 T2 vs T1 T3 vs T2 
PVR (dyne s cm–5 m–2258 (159) 202 (85) 272 (116) 189 (93) 262 (136) 184 (74) NS  NS  
Variable T1 T2 T3 ANOVA results 
 Group L  Group O Group L Group O Group L Group O Group L Group O 
MAP (mm Hg) 84 (13) 92 (12) 84 (8) 108 (19)* 83 (8) 96 (13) NS  T2 vs T1 T3 vs T2 
HR (beats min–173 (12) 82 (14) 73 (11) 80 (15) 74 (10) 78 (13) NS  NS  
RAP (mm Hg) 9.0 (4.6) 7.6 (3.2) 7.4 (4.6) 6.0 (1.8) 9.5 (6.0) 6.6 (3.4) 0.12  0.13  
PAOP (mm Hg) 11.5 (4.7) 11.3 (2.0) 11.5 (5.5) 10.1 (2.0) 12.8 (5.2) 11.2 (3.4) NS  NS  
MPAP (mm Hg) 21 (6) 20 (2) 20 (5) 18 (3) 23 (7) 20 (5) T3 vs T2  NS  
CI (litre min–1 m–23.6 (1.5) 3.8 (1.2) 2.8 (1.3) 3.6 (1.9) 3.5 (1.1) 3.7 (1.1) T2 vs T1 T3 vs T2 NS  
SVR (dyne s cm–5 m–21846 (520) 1899 (596) 2480 (779) 2705 (1330) 1797 (489) 2062 (569) T2 vs T1 T3 vs T2 T2 vs T1 T3 vs T2 
PVR (dyne s cm–5 m–2258 (159) 202 (85) 272 (116) 189 (93) 262 (136) 184 (74) NS  NS  

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