British Journal of Radiology (2004) 77, 547-550
© 2004 British Institute of Radiology
doi: 10.1259/bjr/19413822
Non-pulsatile hepatic and portal vein waveforms in patients with liver cirrhosis: concordant and discordant relationships
M Barakat, MD
Department of Tropical Medicine and Gastroenterology, Faculty of Medicine, Assiut University, Assiut, Egypt
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Abstract
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The relationship between hepatic vein waveform and portal vein waveform (HVW and PVW) was evaluated in 54 healthy subjects and 148 patients with liver cirrhosis and portal hypertension using spectral Doppler ultrasound recordings. In all healthy subjects, the HVW was triphasic and the PVW was slightly pulsatile. 51 of 148 patients (34.5%) had flat non pulsatile HVW with a significantly higher incidence in Child C vs Child A patients (48.9% vs 20.7%, respectively; p<0.01) while 56 of 148 patients (37.8%) had flat PVW, also with significantly higher incidence in Child C vs Child A patients (46.7% vs 25.9%, respectively; p<0.05). Of the 86 patients having flat waves (HVW or PVW), only 21 (24.4%) had concordant flat waves (flat both HVW and PVW) while discordance was detected in the remaining 75.6% patients. Only 22 patients (14.9%) had a triphasic HVW but with broad spectrum and absent window in 20 (90.9%) and significantly lower pre-systolic:systolic (PS) ratio (Vmax of the pre-systolic retrograde wave/Vmax of the systolic antegrade wave) compared with healthy subjects (0.23±0.1 vs 0.42±0.18, respectively; p<0.001). In conclusion, spectral broadening with window absence and dampening of the retrograde pre-systolic wave mark are the earliest changes in HVW in cirrhotic patients even in the presence of a triphasic pattern. The transmission of hepatic vein pulsatility is not a major factor responsible for portal vein pulsatility.
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Introduction
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With the availability of Doppler ultrasound, attempts have been made to study various blood flow characteristics in patients with liver cirrhosis and portal hypertension, using simple and non-invasive techniques [1]. As a qualitative parameter, inspection of the flow waveform on spectral analysis can give information regarding the existence of flow changes [2]. For example, while the hepatic vein waveform is normally triphasic, dampening of the pulsatility pattern even to a flat trace has been demonstrated in patients with liver cirrhosis [3]. Similarly, although the portal vein waveform is only slightly pulsatile, decreased pulsatility has also been described in cirrhotic patients and may eventually become flat wave [4]. However, there are no available data describing the simultaneous waveform changes in both vessels. The aim of this work was to evaluate the relationship between hepatic vein and portal vein waveforms in cases of liver cirrhosis and portal hypertension particularly when a non pulsatile flat flow pattern prevails.
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Subjects and methods
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The study included 148 patients with hepatic cirrhosis and portal hypertension (87 men and 61 women) with an age range of 19–65 years (mean±standard deviation (SD): 44.7±11.2 years). The diagnosis of cirrhosis was based on a combination of clinical data (e.g. jaundice, ascites, muscle wasting, cutaneous spider angiomas, ecchymosis, palmar erythema and flapping tremors), laboratory data (e.g. decreased serum albumin and prolonged prothrombin time), and ultrasound data (e.g. coarsened bright liver echopattern and nodular liver surface), in addition to liver biopsy whenever possible. Grading of the severity of liver cirrhosis was according to the Child classification modified by Pugh [5]. This classification system is a score of the clinical and laboratory findings including the presence of ascites, the grade of encephalopathy, serum bilirubin and albumin, and prothrombin time. 58 patients were allocated into Child-Pugh class A, 45 into class B and 45 into class C, where class C represents the most pronounced liver dysfunction. The aetiology of their cirrhosis was hepatitis B or hepatitis C, none of the patients were alcoholic. All patients included in the study had oesophageal varices demonstrated on upper endoscopic examination confirming the presence of portal hypertension. Exclusion criteria were (1) portal vein thrombosis, (2) reversed portal vein flow, (3) previous sclerotherapy, band ligation or any surgical intervention that can alter the hepatic haemodynamics, and (4) grade 3 or 4 encephalopathy, preventing co-operation during Doppler examination. In addition, 54 healthy subjects were examined as a control group; 30 men and 24 women with an age range of 18–59 years (mean±SD: 32.8±9.1 years). The healthy subjects were asymptomatic with no history of hepatic or cardiac diseases and with normal liver ultrasound appearance.
Doppler ultrasound examination was performed for all patients and healthy adults (Acuson XP10, Acuson Corporation, USA) using a vector transducer operating at 3.5 MHz. The portal vein flow waveform was recorded at a point midway between the confluence of the splenic and superior mesenteric veins and the bifurcation of the portal vein with the transducer oriented along the longitudinal axis of the main portal vein through a paramedian or slightly oblique plane. The hepatic venous waveform was recorded from the middle hepatic vein at a point 2–3 cm away from the inferior vena cava.
The Doppler angle (between the axis of the Doppler beam and that of the vein examined) was always <60°. The sample volume was adjusted to include as much of the lumen as possible without including the vessel wall. All examinations were performed on fasting subjects and during suspended expiration. Description of the flow waveform was made after producing a frozen spectral strip. The portal vein waveform was described as PV0 when the wave was slightly pulsatile (i.e. showing variation of the peak velocity with time along the wave envelope), or PV1 when the wave envelope was almost flat (Figure 1
). According to the classification of Bolondi et al [3], the hepatic vein waveform was described as HV0 when it was triphasic, HV1 when it showed decreased oscillations with absent reversed pre-systolic wave, and HV2 when the wave was almost flat (Figure 2). Whenever the HV0 pattern was recorded, the pre-systolic:systolic ratio (PS ratio) was calculated as follows: Vmax (maximum velocity) of the pre-systolic retrograde wave/Vmax of the systolic antegrade wave.
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Figure 1. Portal vein waveform patterns. (a) PV0 with a slightly pulsatile envelope. (b) PV1 with a flat envelope.
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Figure 2. Hepatic vein waveform patterns. (a) A triphasic HV0 pattern (two antegrade waves below the baseline and one pre-systolic retrograde wave above the baseline) with a narrow spectrum and a visible window. (b) HV1 with absent reversed pre-systolic wave. (c) HV2 with a flat pattern.
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Statistical analysis
2 test was used to examine differences in distribution of the different wave patterns between the study groups. Probability values <0.05 were considered significant.
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Results
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The hepatic vein and portal vein flow waveforms are shown in Tables 1 and 2. The hepatic vein waveform was triphasic (HV0) in all healthy subjects (100%) with a narrow spectrum and visible window in 48 (88.9%). The PS ratio was 0.42±0.18 (mean±SD). In the cirrhotic patients, this triphasic pattern was seen in only 22 (14.9%) but with a broad spectrum and absent window in 20 of them (90.9%), and a significantly lower PS ratio compared with healthy subjects (0.23±0.1; p<0.001) (Figure 3). Conversely, while a flat hepatic vein waveform (HV2) was not seen in any of the healthy subjects, it was present in 51 of the liver cirrhosis patients (34.5%) with a significantly higher incidence in Child C (48.9%) compared with Child A patients (20.7%); p<0.01.
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Figure 3. Triphasic hepatic vein waveform (HV0) in a cirrhotic patient but with spectral broadening, absent window and a very small reversed pre-systolic wave above the baseline.
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The portal vein waveform was slightly pulsatile (PV0) in all healthy subjects. A flat waveform (PV1) was seen in 56 of the liver cirrhosis patients (37.8%), also with a significantly higher incidence in Child C vs Child A patients (46.7 vs 25.9%, respectively; p<0.05).
Of the 86 patients in whom flat waves were recorded (in the hepatic or portal vein), only 21 (24.4%) had concordant flat waves (flat both hepatic vein waveform and portal vein waveform) while discordance was detected in the remaining 75.6% (65 patients) who had either flat hepatic vein waveform alone (30 patients) with a pulsatile portal vein waveform (PV0); or flat portal vein flow wave alone (35 patients) with a still pulsatile hepatic vein wave (HV0 or HV1).
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Discussion
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The normal hepatic vein flow wave is triphasic and hence a qualitative way of assessment of its form is dependent on evaluating the change in this phasic pattern. In patients with chronic liver disease, grading systems have been designed for the recorded waveform on spectral Doppler ultrasound display. For example, three grades (HV0–HV2) were described by Bolondi et al [3] to cover the change from the normal triphasic form to the flat pattern, while six grades were suggested by Ohta and colleagues (HV1–HV6) to give more detail, down to the complete absence of the wave [6]. Despite having more than one grading system, the first deviation from normality was pointed to by a loss of the reversal phase (the pre-systolic reversed wave). As demonstrated in this study, the triphasic pattern was still preserved in 14.9% of the cirrhotic patients. However, in those patients having the seemingly normal triphasic pattern, dampening of the reversed wave in comparison with normal subjects was clear both on general inspection of the waveform and also on the calculated numerical figures of the PS ratio. Haemodynamically, this is a logical sequence of events for a reversed wave to be dampened before being completely absent. Although the qualitative type of assessment is easier and taken to be more reliable, rapidly informative and less subjective to errors than the quantitative measurements [7], the wide haemodynamic ranges in both normal and disease conditions may mask some of the intermediate changes if only one type of assessment is considered. Thus, to take both into consideration (i.e. qualitative and quantitative measurements) would be more informative at least on trying to assess and follow up the various sequential changes related to disease progression. Furthermore, spectral broadening with complete absence of a window area (between the wave components and the base line) is another point to be taken into account on qualitative assessment of the hepatic vein waveform particularly in those patients having the normally appearing triphasic pattern. The window was absent in 90.9% (20/22) of the patients having the triphasic pattern compared with only 11.1% (6/54) of the normal subjects. In cirrhotic patients, the spectral broadening can be haemodynamically explained as a step preceding dampening of the wave and absence of the reversed component, due to extension of the low velocity streams in the recorded waveform. On the other hand, broadening of the spectrum in a minority of the normal individuals may be related to some unidentified physiological factors, especially when the other wave characters, including the PS ratio, are normal and there is no evidence of a liver disease.
A similar phenomenon of spectral broadening in the portal vein waveform was shown in chronic liver disease patients in an earlier study together with a decrease in the pulsatility index [4]. As an extension to that work, the portal vein pulsatility was viewed in this study through a qualitative assessment of the waveform as either having a pulsatile (PV0) or flat envelope (PV1). This was attempted both to avoid calculations and to give an easy expression which can correspond to the widely accepted way of describing the hepatic venous waveform patterns. Portal vein pulsatility has been assumed to be related, at least in part, to the retrograde transmission of the hepatic vein pulsatility. This is supported by increased portal venous pulsatility in cases of tricuspid regurgitation [8]. In this study, a trial was made to examine this relationship between hepatic and portal vein pulsatility patterns in cases of cirrhosis where the existing histopathological changes, particularly fibrosis, would result in dampening of the hepatic vein flow wave due to loss of pliability of the venous wall [3]. As shown in the results, although the occurrence of non pulsatile flow patterns in the hepatic or portal vein tracings tend to increase with progression of the liver disease (from Child-Pugh class A to C), however, the association between flatness of the hepatic venous wave and that of the portal vein is not parallel. Only a quarter of cases had concordant flat waves in both the hepatic and portal veins. With this situation, if the lack of hepatic vein pulsatility was taken to explain the non pulsatile portal vein waveform, then what would explain the other two remaining discordant haemodynamic patterns? In other words the first pattern of having a still pulsatile portal vein flow despite a complete flatness of the hepatic venous wave, and the other pattern of a flat portal vein wave with a still pulsatile flow in the hepatic vein.
The existence of such discordant relationships proves that the effect exerted by the hepatic vein pulsatility is not a major factor responsible for portal vein pulsatility. Some other factors have been suggested to play a role in portal vein pulsatility such as transmission of splanchnic arterial pulsations, hepatic artery and inferior vena cava pulsations [9], although the exact relationship of these factors has not been determined. Moreover, in patients with cirrhosis, additional factors have to be considered particularly in view of the consequent circulatory changes. One of these factors is the extended portal venous territory resulting from opening of collateral channels [10], which is expected to modulate the portal vein pulsatility. However, the degree of collateralization shows variation among patients and hence the modulatory effect of this phenomenon on portal vein pulsatility is not consistent, leading in turn, to this discordant pattern in relation to hepatic vein pulsatility changes. Also, the interacting and still inconsistent effect of various circulating humoral factors, e.g. glucagon, nitric oxide, prostaglandins, and gastrointestinal peptides, on both the splanchnic arterial and portal venous beds would change the portal venous flow pulsatility and can give a further explanation for the discordant patterns [11–14].
In conclusion, flat non pulsatile patterns tend to increase with progression of the liver disease both in relation to the portal vein and hepatic vein waveforms. However, the change is not parallel confirming that transmission of the hepatic vein pulsatility is not a major factor responsible for portal vein pulsatility. Spectral broadening with window absence and dampening of the retrograde pre-systolic wave mark the earliest changes in hepatic vein waveforms in liver cirrhosis patients even in presence of a triphasic pattern.
Received for publication March 11, 2003.
Revision received November 25, 2003.
Accepted for publication March 22, 2004.
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References
|
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- Partiquin H, Lafortune M, Burns P, Dauzat M. Duplex Doppler examination in portal hypertension: technique and anatomy. AJR Am J Roentgenol 1987;149:71–6.[Abstract/Free Full Text]
- Kremkau FW. Doppler principles. Semin Roentgenol 1992;27:6–16.[CrossRef][Medline]
- Bolondi L, Bassi S, Gaiani S, Zironi G, Benzi G, Santi V, et al. Liver cirrhosis: changes of Doppler waveform of hepatic veins. Radiology 1991;178:513–6.[Abstract/Free Full Text]
- Barakat M. Portal vein pulsatility and spectral width changes in patients with portal hypertension: relation to the severity of liver disease. Br J Radiol 2002;75:417–21.[Abstract/Free Full Text]
- Pugh RNH, Murray-Lyon IM, Dawsan JL, Pietroni MC, Williams R. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg 1973;60:646–9.[Medline]
- Ohta M, Hashizume M, Tomikawa M, Ueno K, Tanoue K, Sugimachi K. Analysis of hepatic vein waveform by Doppler ultrasonography in 100 patients with portal hypertension. Am J Gastroenterol 1994;89:170–5.[Medline]
- Taylor KJW, Holland S. Doppler US. Part I. Basic principles, instrumentation and pitfalls. Radiology 1990;174:297–307.[Abstract/Free Full Text]
- Abu-Yousef MM, Milam SG, Farner RM. Pulsatile portal vein flow: a sign of tricuspid regurgitation on duplex Doppler sonography. AJR Am J Roentgenol 1990;155:785–8.[Abstract/Free Full Text]
- Gallix BP, Taourel P, Dauzat M, Bruel J-M, Lafortune M. Flow pulsatility in the portal venous system: a study of Doppler sonography in healthy adults. AJR Am J Roentgenol 1997;169:141–4.[Abstract/Free Full Text]
- Rousselot LM, Moreno AH, Panke WF. Studies on portal hypertension. The clinical and physiologic significance of self established (non surgical) portal systemic venous shunts. Ann Surg 1959;150:384–410.[Medline]
- Bosch J, Pizcueta MP, Fernandez M, Feu F, Cirera I, Luca A, et al. Hepatic splanchnic and systemic haemodynamic abnormalities in portal hypertension. Ballieres Clin Gastroenterol 1992;6:425–36.[CrossRef][Medline]
- MacMathuna P, Vlavianos P, Westaby D, Williams R. Pathophysiology of portal hypertension. Dig Dis 1992;10(Suppl. 1):3–15.
- Shah V, Garcia-Cardena G, Sessa W, Groszmann RJ. The hepatic circulation in health and disease: report of a single-topic symposium. Hepatology 1998;27:279–88.[CrossRef][Medline]
- Dagher L, Burroughs A. Variceal bleeding and portal hypertensive gastropathy. Eur J Gastroenterol Hepatol 2001;13:81–8.[CrossRef][Medline]
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Abstract
Introduction
