Liver cirrhosis is a well-known clinical entity that has a worldwide distribution with no discernable difference in gender and race, albeit having multiple etiologies; it might have the same longstanding consequences and complications like portal hypertension and hepatic decompensation. It had been agreed that the gold standard reference for the assessment of the degree of cirrhosis is the histological analysis obtained by liver biopsies; however, it should not be the standard care for all cirrhotic patients, being an invasive procedure especially in patients with hemorrhagic tendency [10].
As liver cirrhosis continues, it may alter the hepatic vascular parameters; thus, the Doppler ultrasound scan is warranted as a primary focus for many researchers to be an alternative investigation that could surrogate such invasive procedures [10].
As we mentioned, MELD score system had outperformed the CTP system in patients with chronic liver disease especially those who are candidates for hepatic transplantation, being more based on objective laboratory biomarkers than do the CTP system; moreover, MELD score does not consider demographic factors like age and race in hepatic transplantation listing; thus, it had been considered as a more favorable scoring system than CTP [1, 3, 10].
On review of literature, the main objective of this study was to evaluate whether there was a correlation between hepatic Doppler parameters as well as the ultrasound findings of hepatic decompensation with the clinical status in cirrhotic patients as measured by MELD score.
In light of our results, we found a statistically significant correlation between the hepatic artery velocity (HAV) and MELD score (Tables 1 and 2) (Figs. 1a, 3, and 4), where 70% of our cases had showed increased HAV.
This was concordant with Park et al. studies who involved 264 cirrhotic patients and had correlated the Doppler parameters with markers for hepatic decompensation and reported a statistically significant correlation between HAV and MELD score (ρ = 0.0001) [11, 12]; Glisic et al. had also concordant supportive results, but with a relatively smaller sample size (80 patients and 20 controls), and they had reported an increase in HAV of cirrhotic patients with an average (125.7 cm/s), compared to their healthy controls (79.3 cm/s) [13]; our results had matched theirs, where the cut-off point was 145 cm/s (Table 5 and Fig. 2c, d).
A literature-based rationale for such results, where the increased hepatic sinusoidal resistance would, in turn, decrease the portal venous inflow; therefore, it activates the hepatic artery buffer response (HABR; mediated by adenosine washout and angiotensin II system) and increases the hepatic arterial inflow as a compensatory mechanism, to maintain consistent oxygen in the hepatic parenchyma; nevertheless, some studies had documented that HABR is maintained in the setting of cirrhosis [14, 15].
Discordance with Azizah et al. study was present in this regard, where they included 56 eligible cirrhotic patients and studied the correlation of hepatic hemodynamics with CTP score, and found that the HAV was not significantly different between the study and the control groups (ρ = 0.06). Their possible reason for the contradicting data was that two different US systems were used to scan both control and study groups. No prior checking was carried out by scanning the same patient/s using these two US scanners to look for any significant difference in the measurement of the studied parameters. Also, they were using the CTP score in classifying their patient population, assessing their prognosis, and to predict their mortality. An important deficiency in the CTP score is that it uses 2 very subjective variables in its calculation, namely portosystemic encephalopathy and severity of ascites, again, MELD score calculation is based on more objective parameters [16].
Portal flow velocity was also a studied parameter, although 59% of our patients showed significantly decreased portal flow velocity (< 20 cm/s) (mean ± SD, 19.68 ± 6.49) (Tables 1 and 2) (Figs. 1b, 3, and 4). We had found that PVV did not significantly correlate with MELD score; this was concordant with many works of literature [16,17,18,19] who had documented the same issue; however, this was contradicting the Berzigotti et al. study, where they reported a low flow velocity of < 20 cm/s in addition to a caliber increase in the main portal vein (MPV) were considered diagnostic features of portal hypertension [20]. However, we did not measure the portal vein diameter, and the possible reason for the contradicting data in the PVV was the heterogeneity of the cirrhotic patients included in various studies, also the type of hemodynamic disturbances, for example, the presence of hyperkinetic syndrome or portosystemic collaterals.
Hepatic artery resistivity index (HARI) was additionally investigated in our present study. We found that HARI did not significantly correlate with MELD score, splenomegaly, or ascites (Tables 2, 3, and 4) (Fig. 1c).
This was matching the study done by Iranpour et al., who had observed a specificity and sensitivity of utilizing a hepatic arterial resistive index (RI) cut-off of > 0.77 to predict cirrhosis were as low as 70% and 68%, respectively [15], further supportive results had been provided by other studies [7, 11, 13].
This was discordant with the Azizah et al. study, where they found that the increased HARI in the liver cirrhosis was statistically significant and it helped in differentiating cirrhotic participants (where HARI values were above 0.7) from the non-cirrhotic ones (HARI values were less than or equal to 0.7). A possible explanation for the contradicting data is that the RI of the hepatic artery can be changed by certain physiological factors and could be elevated shortly after meal ingestion, where the portal vein flow increases then a corresponding reduction in the arterial flow was induced by vasoconstriction. Nevertheless, the state of vasoconstriction could result in a transient elevation of RI that could last up to few hours [21, 22]; this is why the HARI should be carefully obtained with special consideration for the physiological variations. In our study, we did instruct all patients for 6 h fasting to avoid this diagnostic bias and we had found no significant correlation.
In the setting of cirrhosis, findings like splenomegaly and ascites could suggest a state of hepatic decompensation, we had depicted a statistically significant correlation between the presence of splenomegaly, MELD score, and HAV; however, this significant correlation was not existing with either PVV or HARI (Table 3)(Figs. 2a, 3, 4). At this extent, we had a concordance with many studies [11, 23,24,25], but on the other hand, it was discordant with the Yadav et al. study [26], who found (out of 112 patients) no significant correlation between MELD score and spleen size in cirrhosis.
Kashani et al. had explained this discordance, where the size of the spleen could vary between cirrhotic patients according to their primary disease etiologies, with hepatitis C virus (HCV) infected and non-alcoholic hepatitis patients were showing significantly larger organ dimensions as compared to those with alcoholic hepatitis [27], almost all of our patients lie in the category of post-infection (hepatitis) cirrhosis, where the splenomegaly was accordingly a harmonious feature. It worth mentioning, that some authors had suggested that splenomegaly is associated with a poor prognosis in cirrhotic patients and could be used as an index for the non-invasive assessment of esophageal varices and bleeding risks during radioactive or acoustic examinations [28, 29].
Ascites is another important complication of cirrhosis and is usually associated with poor prognosis (1- and 5 year moralities are 15% and 44%, respectively), on follow-up [30].
The current study showed a statistically significant correlation between the presence of ascites and the MELD score as well as HAV. But on the other side, the correlation with both PVV and HARI (Tables 2 and 4) (Figs. 2b and 4) was statistically insignificant; this was in line with Azizah et al., Park et al., and Somsouk et al. studies [11, 16, 30].
Yet, Popov et al. had evaluated and compared the changes of hepatic and renal Doppler parameters in cirrhotic patients, and found no significant differences between hepatic Doppler parameters and the presence or absence of ascites [31]. Our explanation for this mismatch was attributed to the different stages of hepatic cirrhosis in their patients who could have a previous taping or had received treatments for ascites. But most of our ascetic patients had a decompensated end-stage liver disease and gave no history of previous surgical intervention or the transjugular intrahepatic portosystemic shunt (TIPS) to treat their ascites.
Although providing potentially useful data, we had some limitations in this work including the following:
First, in this study, we did not correlate the degree of cirrhosis or confirm the presence of cirrhosis on histologic bases. Although we agree that histology is considered a reference standard, it was not the standard protocol to have a hepatic biopsy in all cirrhotic patients. Second, we did not include normal controls in our study, as we consider that the MELD score has only been used in cirrhotic patients and is not validated to be used in normal individuals. Moreover, normal individuals do not have regularly checked laboratory tests for MELD to provide a fair comparison. Third, is that our study sample was from a single center. Finally, the study duration was relatively short (about 12 months) with a relatively small sample size of recruited patients; therefore, statistical analysis may not be so robust.