Objectives: Our aim was to investigate the early changes that occur after graft perfusion in living-donor liver transplant by Doppler ultrasonography.

Materials and Methods: We prospectively evaluated liver grafts of 30 patients who underwent living-donor liver transplant during an 18-month period and who were followed for 1 year postoperatively. The hepatic artery peak systolic velocity, resistivity index, portal vein velocity, portal vein anastomotic velocity ratio, and hepatic vein pattern were compared after excluding patients who developed vascular com­plications and acute rejection episodes.

Results: We observed intraoperative increases in the mean hepatic artery peak systolic velocity (96.3 ± 65 cm/s), the resistivity index (0.78 ± 0.091), and the portal vein velocity (99.6 ± 48 cm/s), which started to normalize after 2 weeks. In comparing the mean portal vein velocity, portal vein anastomotic velocity ratio, hepatic artery peak systolic velocity, and resistivity index after excluding 5 patients who developed vascular complications, we observed overall significance levels of P < .001, P = .039, P < .001, and P = .040. After we excluded 9 patients who developed acute rejection, our comparison of the portal vein velocity, hepatic artery peak systolic velocity, and resistivity index showed overall significance (P < .001, P < .001, and P = .043).

Conclusions: Early and transient increases in portal vein velocity, anastomotic velocity ratio, hepatic artery peak systolic velocity, and resistivity index are common after living-donor liver transplant, with significant declines in the first 2 weeks posttransplant.

Key words : Duplex, Hepatic, Perfusion, Perioperative, Recipients

Introduction

Doppler ultrasonography is often utilized in the perioperative assessment of recipients during living-donor liver transplant (LDLT), with an ability to provide quantitative analyses of graft hemodynamic variables. The value of Doppler ultrasonography in the early diagnosis of vascular complications after liver transplant has been previously established.^1,2 However, the immediate changes in the splanchnic hemodynamics after graft perfusion and the physiologic changes during graft recovery are still under debate.³ Few reports have investigated early graft hemodynamics by using Doppler ultraso­nography after LDLT, with hemodynamics with LDLT influenced by the complex vascular anasto­mosis and small graft volume compared with deceased-donor liver transplant (DDLT).

The aim of this work was to evaluate the role of Doppler ultrasonography in monitoring the peri­operative graft hemodynamics in adult donor-adult recipient LDLT and to clarify the normal or physiologic changes that occur intraoperatively and during the early postoperative period. We compared the mean of the different Doppler parameters after excluding patients who developed vascular com­plications and acute rejection episodes.

Materials and Methods

Approval of this study was obtained from our institutional review board, which was in accordance with the Declaration of Helsinki, and informed consent was obtained from all patients. We prospectively evaluated 30 consecutive patients who underwent adult-adult LDLT during an 18-month period by Doppler ultrasonography with 1-year postoperative follow-up. All recipients had hepatitis C-related cirrhosis and received right lobe graft from a living related donor.

Doppler ultrasonography examinations were performed using an ultrasonographic scanner (Siemens Sienna and Siemens G60; Siemens AG, Munich, Germany) with a 3.5- to 5-MHz convex probe. The wall filter was set at 50 to 100 Hz; the sample size was maintained below 5 mm and was located at the center of each vessel. The spectral waveform was angle corrected, and the Doppler angles of incidence were less than 60°. Intraoperatively, a sterilized intraoperative linear probe (T shaped) with central frequency of 7.5 to 10 MHz was used.

Preoperative doppler ultrasonography
To evaluate the degree of portal hypertension, we assessed the portal vein (PV) diameter, patency, flow velocity and direction of flow, size of the spleen in long axis, and amount of ascites. Other findings, such as hepatic focal lesions, gall bladder stones, nephro­pathy, and pleural effusion, were also collected.

Intraoperative ultrasonography
Intraoperative ultrasonography was routinely per­formed before biliary anastomosis. Scanning was performed several minutes after the arterial anastomosis was finished to allow for the immediate hemodynamic changes after reperfusion to be established and for the hepatic artery (HA) to recover from spasticity.

For HA evaluation, size mismatches between recipient and donor HA were measured by gray-scale ultrasonography and graded as follows: mild mismatch < 25% luminal reduction, moderate mismatch = 25% to 50% reduction, and significant mismatch = 50% to 75% reduction. The HA peak systolic velocity (PSV) was measured before, during, and after anastomosis. The anastomosis-to-pre­anastomosis velocity ratio and mean PSV were calculated. An examination of the intrahepatic arterial waveform was then performed. The resistivity index (RI) was used as an indicator for the peripheral vascular resistance (RI = PSV – end diastolic velocity/PSV). We estimated the degree of HA anastomotic stenosis depending on the size mismatch and the anastomosis-to-preanastomosis velocity ratio and detected the intrahepatic damped signal (tardus parvus waveform). Anastomotic flow jet (2- to 3-fold compared with preanastomotic flow) was considered a normal finding in the presence of size mismatch and kinks and as a normal intrahepatic waveform pattern. A high anastomotic jet (> 3-fold) with high-pitched sound and damped intrahepatic PSV and increased systolic acceleration (tardus parvus waveform) were considered as signs of HA stenosis.

For PV evaluation, the whole length of the recipient’s PV was examined for remnants of thrombi. The size mismatch between the recipient and donor PV was graded as mild mismatch (< 25% luminal reduction), moderate mismatch (25%-50% reduction), and significant mismatch (> 50% reduction). The PV velocities before, during, and after anastomoses were measured. The anastomotic-to-pre-anastomotic velocities and the mean PV velocities were calculated.

For hepatic vein evaluation, waveforms were classified into triphasic waves in which a retrograde flow was observed in the first phase followed by antegrade flow in the subsequent 2 phases, with biphasic waves as those in which no retrograde flow was observed and monophasic flow showing no pulsation. Assessment of venous grafts or accessory veins was performed when present. Absolute velocity values and anastomotic velocity ratios were reported whenever there was suspicion about the hepatic vein anastomosis integrity or graft torsion.

Postoperative doppler ultrasonography
In our institution, routine Doppler ultrasonography evaluation of the hepatic circulation is performed twice daily during the first week and once daily during the rest of the hospital stay. After hospital discharge, Doppler ultrasonography evaluation is done on weekly basis during the first 3 months, then monthly until the end of 6 months, and finally every 2 months or according to the clinical condition.

For HA evaluation, flow was studied at ex­trahepatic and intrahepatic levels (anterior segmental branch), and the mean was calculated. The PSV was measured at a straight segment of the HA to minimize errors due to angle correction or kinking of the artery. The intrahepatic velocity was measured usually in the anterior branch of the HA using longitudinal intercostal scanning. The posterior branch was not selected because the angle of incidence tends to be larger than 60°. The RI was then calculated.

For PV evaluation, diameters of recipient and donor PV and the diameter of the anastomosis were measured by gray-scale ultrasonography. Portal vein waveforms were obtained before, during, and after anastomosis. The mean PV velocities and the anastomotic-to-preanastomotic velocity ratio were calculated.

For hepatic vein evaluation, waveform patterns were described as monophasic, biphasic, and triphasic.

Statistical analyses
For statistical purposes, the different Doppler parameters were measured at day 1, after 1 week, at 2 and 3 weeks, and at 1 year postoperatively.

To investigate the normal or physiologic peri­operative graft hemodynamics, we compared the mean of the following Doppler parameters for the study period: HA PSV, HA RI, PV velocity, and anastomotic-to-preanastomotic velocity ratio, after excluding patients who developed vascular com­plications. We then compared the mean HA PSV, HA RI, and PV velocity, after excluding patients who developed acute rejection episodes during the study period.

Data were statistically described in terms of range, means and standard deviation, frequencies (number of cases), and relative frequencies (percentages) when appropriate. Comparison of quantitative variables between different groups was done using Mann-Whitney U test for independent samples. Comparison of quantitative variables over the study period was done using the Freidman test with post hoc multiple 2-group comparisons. Categorical data were compared using the chi-squared test. An exact equation was used instead when the expected frequency was < 5. A probability value (P value) of < .05 was considered statistically significant. All statistical analyses were performed using the computer program Microsoft Excel version 7 (Microsoft Corporation, New York, NY, USA) and SPSS (Statistical Package for the Social Science; SPSS Inc., Chicago, IL, USA) for Windows.

Results

This study included 30 consecutive transplant recipients, made up of 29 male patients (96.6%) and 1 female patient (3.4%). Ages ranged from 38 to 63 years old (mean of 49.8 ± 5.9 years). Donor age ranged from 21 to 46 years old (mean of 32 ± 7.4 years), with 24 male (80%) and 6 female donors (20%). Graft-to-recipient weight ratio ranged from 0.8 to 1.4 (mean of 1.02 + 1.3).

Preoperative doppler ultrasonography results
Six patients (20%) had hepatic focal lesions (hepatocellular carcinoma) in their cirrhotic livers. One patient developed acute partial PV thrombosis 1 week before surgery, which resolved preoperatively with medical treatment.

The PV diameters ranged from 6 to 17 mm (mean [standard deviation, SD] diameter = 13.2 [2.5] mm) and portal vein velocities ranged from 10 to 35 cm/s (mean [SD] velocity = 13.4 [9] cm/s). Spleen sizes ranged from 14 to 21 cm in long axis (mean [SD] size = 17.4 [2.8] cm). Nine patients (30%) had mild ascites, 9 patients (30%) had moderate ascites, 5 patients (16.7%) had marked ascites, and 7 patients (23.3%) had no ascites. Five patients (16.7%) had mild pleural effusion.

Intraoperative doppler ultrasonography results
In the HA, mild size mismatch (> 25%) was detected in 25 patients (83.3%), moderate mismatch (25%-50%) in 4 patients (13.3%), and significant mismatch (> 50%) in 1 patient (3.3%), which was diagnosed as HA stenosis based on the increase in the anastomotic velocity (5-fold) and damped intrahepatic waveform (tardus parvus waveform). Successful revision of the anastomosis was performed.

There were initial increases in PSV (range, 20-300 cm/s; mean [SD] PSV = 96.3 [65] cm/s), in RI (range, 0.61-0.98; mean [SD] RI = 0.78 [0.091]), and in the anastomotic-to-preanastomotic velocity ratio (range, 1-5; mean [SD] = 1.32 [0.56]). Twelve patients (40%) had high RI > 0.8, and 18 patients (60%) had normal RI < 0.8 (with RI = 0.8 as a cut-off value). Six patients improved after local application of vasodilator. Proximal dissection of the recipient HA occurred in 3 patients with moderate mismatch and diseased recipient arteries; dissections were self-limiting with no complications.

In the portal vein, mild size mismatch (< 25% luminal reduction) was detected in 22 patients (73.3%), moderate mismatch (25%-50%) in 7 patients (23.3%), and significant mismatch (60%) in 1 patient (3.3%).

There was initial increase in the portal flow velocities (range, 18-236; mean [SD] velocity = 99.6 [48] cm/s) and in the anastomotic-to-preanastomotic velocity ratio (range, 1-4; mean [SD] = 1.82 [0.95]).

In the hepatic veins, a triphasic pattern was seen in 23 patients (76.7%) and a biphasic pattern in 7 patients (23.3%). Four patients had right inferior hepatic veins anastomosed to the inferior vena cava. Two patients had segment VIII vein anastomosed separately with the inferior vena cava.

Postoperative Doppler ultrasonography results
Postoperative complications were divided as early complications (during hospital stay) and late complications (during year 1 postoperatively), with results summarized in Table 1.

The mean of the different Doppler parameters (HA PSV, HA RI, PV velocity, PV anastomotic velocity ratio) and the hepatic vein patterns for the 30 patients are summarized in Tables 2 and 3.

There were 3 mortalities 8 and 9 months after transplant: 2 patients from acute rejection and 1 from sepsis. Five patients developed vascular complications, with 3 having clinically silent PV stenosis (50%-60%) and 2 developing early hepatic artery thrombosis. Three patients were diagnosed as PV stenosis, with 2 at 50% stenosis and 1 at 60% stenosis with mild size mismatch by intraoperative ultrasonography. The diagnosis was based on Doppler ultrasonographic criteria: reduction of the vessel lumen by 50% or more at the site of narrowing relative to the prestenotic area or when the caliber of the vessel is 5 mm or less at the site of narrowing. In addition, the criteria also include velocity in the stenotic segment that is 3 to 4 times greater than that in the prestenotic segment. None of the patients developed mani­festations of portal hypertension and were treated conservatively.

Two patients were diagnosed as having hepatic artery thrombosis on the basis of Doppler ultra­sonographic results. For the first patient at day 4 after transplant, we relied on the sign of impending thrombosis initially described by Nolten and Sproat.4 There was absent diastolic flow and damped systolic peak in absence of manifestations of graft dysfunction. In the first patient, intra-arterial thrombolysis was initially successful; however, rebound thrombosis developed due to an adherent thrombus and size mismatch, provoking rethrom­bosis and successful surgical reconstruction. In the second patient, hepatic artery thrombosis developed on day 3 postopera­tively; intra-arterial thrombolysis was suc­cessful in resolving the thrombus and showed the underlying anastomotic stricture; further balloon angioplasty and stent placement were also required.

After excluding 5 patients who developed postoperative vascular complications, we compared the mean HA PSV and RI, which were both significant at P < .001 and P = .040 (Figure 1A and Figure 2A). When we comparing the mean PV velocities and PV anastomotic-to-preanastomotic velocity ratio, we observed overall significance of P < .001 and P = .039 (Figure 3A, Figure 4, and Table 4).

Nine patients (30%) developed acute rejection episodes with clinical evidence of graft dysfunction, which was proven by biopsy. Two patients developed early acute rejection, and 7 patients developed delayed acute rejection episodes during the first year after transplant. After we excluded the 9 patients with acute rejection, our comparison of HA PSV and HA RI showed overall significance (P < .001 and P < .043) (Figure 1B and Figure 2B). Our comparison of the PV velocity over the study period showed an overall significance (P < .001).

Discussion

Early detection of hemodynamic abnormalities after liver transplant requires knowledge of the normal or physiologic changes that immediately accompany the graft perfusion and in the early postoperative period. Immediately after liver transplant for patients with cirrhosis, the mechanical component of portal hypertension is relieved by the healthy graft but without immediate restoration of the systemic or the splanchnic circulation to normal function.⁵ The splanchnic circulation shows rapid and potentially reversible changes in the portal and arterial perfusion and may not be clinically significant.^3,6,7

In LDLT, the hemodynamic changes are much more pronounced than in DDLT, with a high perfusion state that is predominantly portal with increases in the PV flow and velocities and increased HA resistance.^8-10 Analysis of Doppler ultrasono­graphic findings may be confusing intrao­peratively and in the early period after transplant due to complex vascular anastomoses, donor-recipient vascular size mismatch, and reduced graft volume. Regarding changes in portal and arterial parameters by Doppler ultrasonography, they are still under debate.

In this study, we found a dramatic intraoperative elevation of the mean PV flow velocities in cirrhotic patients (mean [SD] velocity = 99.6 [48] cm/s) with significant elevation compared with the preoperative velocities (P < .001) followed by a short period of normalization within the first 2 weeks after transplant (P < .001) (Figure 3). This elevation can be attributed to the persistence of the hyperkinetic hemodynamic splanchnic circulation in patients with cirrhosis and portal hypertension, as agreed on in previous reports.5-7 Other theories that may explain the PV flow elevation in LDLT include reduction in liver vasculature and small PV anastomotic stoma, which could elevate PV resistance and pressure, the effect of loss of sympathetic hepatic innervation, or elevated cardiac output.^9,11,12

Previous studies on whole liver transplant have shown similar but less profound increases in the PV velocities in the immediate and early period after transplant, with variable timing of normalization. A wide range of PV velocities (15-400 cm/s) have been reported in the immediate period after orthotopic liver transplant in patients without vascular complications.1 In their study of 41 patients with cirrhosis, Bolognesi and associates found that the PV velocity increased immediately after DDLT and that high portal velocity was present for 2 years after transplant.⁷ However, Han and associates found a marked reduction in PV velocity in their 144 DDLT recipients, with mean [SD] velocity = 72.1 [30.3] cm/s at 1 day after transplant versus mean [SD] velocity = 44.2 [20.1] cm/s at 1 month after transplant (P < .05).3 In addition, in a series on 51 DDLT recipients, Stell and associates found that the mean portal venous flow decreased by approximately 20% in the first postoperative week.¹

Previous studies have reported marked hemo­dynamic changes after reperfusion of a partial graft in LDLT versus those occurring in DDLT.8 Eguchu and associates studied 13 LDLT patients and found elevated mean PV velocities during the first 3 months after transplant, with higher velocities in the cirrhotic group than in the noncirrhotic group.13 In their study on 14 consecutive donor-recipient pairs, Gondolesi and associates found that the PV velocity/flow dramatically increased 1 hour after reperfusion (94.7 ± 28.4 cm/s; P = .004), with return to baseline 3 months after transplant (58.8 ±37.8 cm/s; P = .01).14 Furthermore, Sugimoto and colleagues studied 10 donor-recipient pairs for 2 weeks after transplant and reported a marked elevation of PV velocity in recipients on the first day after transplant (106.3 ± 45.2 cm/s). Portal vein velocities were significantly higher in recipients than in donors on each postoperative day.¹⁵

Jiang and associates compared differences between graft hemodynamics in 42 DDLT and 20 LDLT recipients. They found that PV flow in patients with cirrhosis and portal hypertension showed a higher perfusion state after LDLT.⁹ In Sainz-Barriga and associates’ comparison between whole and partial liver recipients in 103 patients, an increase in PV flow after graft implantation was observed, with LDLT recipients showing the highest compliance to portal hyperperfusion.¹⁰

In this study, we noticed benign intraoperative elevation of the PV anastomotic-to-preanastomotic velocity ratio (range, 1-4, mean of 1.82 ± 0.95) that was reversible with significant decline in the first week after transplant (P = .039) (Figure 4) without clinical significance or signs of portal hypertension. The anastomotic narrowing and the velocity elevation in the early postoperative period can be attributed to the size mismatch, which was present in more than 96% of cases, in addition to anastomotic edema, which contributes to downstream turbulence and flow vortices. Intraoperatively in borderline cases with questionable stenosis, we rely on measuring the PV pressure gradient across the anastomosis and we consider a gradient > 5 mm Hg to be significant and requiring surgical revision. Three patients in our series with potential PV stenosis (50% and 60%) did not develop signs of portal hypertension and were treated conservatively. We limited the use of invasive transhepatic portography and angioplasty to patients who demonstrated clinically manifesting symptoms.

When a suboptimal graft-to-recipient weight ratio is accompanied by high portal flow in LDLT, hyperperfusion injury and small for size syndrome may result, for which the portal flow should be modulated.^8,16 Doppler ultrasonography parameters may not be sufficient alone, and portal venous pressure measurements will be essential in such conditions. Portal venous pressure has been considered the most important hemodynamic factor influencing the functional status of the liver and graft regeneration after liver transplant. A portal venous pressure of more than 20 mm Hg in the early period after LDLT showed a close association with morbidity and poor graft function.¹⁷

A high-resistance HA flow was a frequent intra­operative finding in our series, occurring in 40% (12/30) of patients, with significant decline in the first 3 weeks after transplant (P = .040 and P = .043), after excluding patients who developed vascular complications and acute rejection episodes. The immediate elevation of the RI intraoperatively could be the result of arterial spasm, which occurred in 50% of patients. Resistivity index improved after local application of vasodilators, whereas persistence of the early high resistance flow has not been associated with worsening of the clinical course or graft dysfunction. The clinical insignificance of this high resistance flow had also been demonstrated in several reports.^4,18-20

Our results agree with the HA buffer response theory in which the HA shows compensatory vasoconstriction reducing the arterial blood flow in response to portal hyperperfusion, thus leading to a high RI.^21,22 This phenomenon had been demon­strated intraoperatively by temporary clamping of the PV, which resulted in improved HA flow.¹⁹ Other theories have related the early and transient elevation of the HA RI after DDLT to the older donor grafts, prolonged period of cold ischemia and preservation injury, graft steatosis, and chronic cholestatic disease as an indication for trans­plant.^18,20,23

In addition, a decreased HA RI (< 0.50) can also be observed in the early postoperative period, although it was less common than a high HA RI. These low HA RI values might be caused by surgical edema, with low HA RI values ordinarily returning to a normal level within 6 months. Low HA RI can also be observed in other pathologic conditions, including HA stenosis, severe aorto-celiac athe­rosclerotic disease, arterio­venous or arterial biliary fistula formation, and hepatic vein or portal vein thrombosis.³

We observed an intraoperative elevation of HA PSV (range, 20-300 cm/s; mean [SD] of 96.3 [65] cm/s) with significant decline in the first day after transplant without long-term consequences. There was also intraoperative elevation of anastomotic-to-preanastomotic velocity ratio (range, 1-5; mean [SD] of 1.32 [0.56]). Because absolute values of the PSV can be influenced by many factors, such as systemic pressure, source of the recipient artery, size mismatch, kinks, spasms, and the high degree of observer variability, we rely more on the intrahepatic (anterior segmental HA) Doppler waveform that describes the true arterial flow reaching the graft. Hence, good intrahepatic flow usually confirms the integrity of the arterial anastomosis.

This study analyzed the spectral Doppler wave­forms in the hepatic veins after LDLT. Two blood flow patterns (triphasic and biphasic waveforms) were detected intraoperatively in hepatic veins of liver recipients, with normal triphasic waveform in most patients (76.7%). The abnormalities in the hepatic vein waveforms were generally considered not specific to diagnosis of hepatic vein stenosis. Graft edema and changes in cardiac output may contribute to abnormal Doppler waveforms in the hepatic vein.3 Quantitative analysis of the hepatic venous flow is essential in the presence of monophasic or damped flow where evaluation of the venous anastomosis and the anastomotic velocity ratio become important to rule out torsion or true anastomotic stenosis.

Limitations of the study are the relatively small sample size and lack of cut-off values to differentiate between normal and abnormal hemodynamic changes after LDLT.

In conclusion, early hemodynamic changes are complex and pronounced after LDLT, with early and transient increases in portal vein velocities, anastomotic velocity ratios, HA velocities, and RI and with significant decline in the first 2 weeks after transplant without long-term clinical consequences. Size mismatches between the recipient and donor hepatic arteries and portal veins are frequent findings and should not be misinterpreted as stenosis. Correlation with operative findings, portal pressure measurements, and clinical condition remain essential for interpretation of the Doppler ultrasonography findings.

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