Reviewer's report
Title:Intrahepatic blood flow assessment by Doppler ultrasonography:
relationship among hepatic vein, portal vein, hepatic artery and portal pressure
intraoperatively measured in patients with portal hypertension
Version: 2Date:11 January 2011
Reviewer: Annalisa Berzigotti
Reviewer's report:
This paper by Zhang and colleagues was aimed at clarifying the
pathophysiological factors associated with abnormalities in hepatic veins Doppler
pattern in patients with cirrhosis and portal hypertension. In 60 patients requiring
surgery for portal hypertension the authors assess simultaneously this Doppler
parameter and portal pressure as measured directly and invasively; they also
measure portal vein velocity and hepatic artery pulsatility index (HAPI) by
Doppler; non-invasive measurements were also performed in a group of healthy
controls.
The results are consistent with a moderate linear correlation between portal
pressure and flattening of flow in the hepatic veins; similarly, portal vein velocity
decreased and HAPI increased in patients with abnormal hepatic vein flow
pattern. It is concluded that in patients with PHT, monophasic HV waveform
indicates higher portal pressure and that it can be hypothesized that
parenchymal fibrosis and fat infiltration reduce HV compliance being the cause of
the abnormality of Doppler HV waveform.
The paper explores an interesting issue, which has been previously evaluated by
other authors but that is still poorly understood. However, the study has some
major limitations, which are listed below:
1) A main flaw of the study is the lack of data about inferior vena cava pressure
and other parameters related to systemic hemodynamics. Absolute portal
pressure is obviously an indicator of the severity of portal hypertension, but from
a pathophysiological point of view the consequences of portal hypertension
depend on the portal pressure gradient, which is calculated as the difference
between portal pressure and inferior vena cava pressure (Bosch et al. Seminars
Liver Diseases 2006). Therefore, the lack of IVC pressure measurement
decreases the reliability of the results.
2) As the authors acknowledge, right heart catheterization or at least
echocardiography should have been performed to rule-out heart valvular
diseases or other conditions which can directly affect HV Doppler pattern.
Moreover, the assessment of cardiac output, systemic arterial pressure and
systemic vascular resistance would have given data on the presence of
hyperdynamic syndrome, which could also be a determinant of abnormality of HV
Doppler flow.
3) The study population is poorly described (see table 1): data on etiology of
cirrhosis, prevalence and size of gastroesophageal varices, previous episodes of
bleeding from varices, ascites, … should be added to support the hypothesis that
abnormalities in HV Doppler pattern depend principally from portal pressure
increase. Indeed, ascites increases intrabdominal pressure which could flatten
HV Doppler pattern.
4) Design of the study: the study lacks a clear hypothesis, which should be better
defined.
5) Study protocol: both portal pressure and central venous pressure can be
affected by drugs used in general anesthesia; the authors should carefully
comment on the protocol of anesthesia used, specifying if this was the same in
all patients, and in which moment PP and Doppler were performed. Were the
patients ventilated? How was respiration suspended?
6) The results show that flattened HV Doppler flow pattern indicated more severe
portal hypertension; however, all patients had severe portal hypertension since
this was an inclusion criteria, and differences in PP between patients with normal
and abnormal flow were very small (2-3 mmHg); how do the authors suggest to
interpret the finding of abnormal HV Doppler pattern in a patients with known
clinically significant portal hypertension? Did the patients with more flattened HV
Doppler pattern show a different outcome on follow-up (decompensation, death,
bleeding…), so supporting a clinical usefulness of the Doppler finding?
7) Discussion: a referral to “liver stiffness” is made in some sentences. In the
methods and results no mention on direct liver stiffness measurement is made;
was liver stiffness evaluated (transient elastography? ARFI? Other methods?) or
is HAPI used as the only surrogate of liver stiffness? If it is so, the authors should
better clarify the background for the use of Doppler impedance of hepatic artery
as an indicator of liver stiffness.
8) Conclusions: Since no correlation was observed between HV Doppler flow
pattern and histological findings it is difficult to accept the conclusion (see last
lines of the abstract), which should be changed.
Minor comments
Histological findings might be better explained in the results section and not only
in table 1; moreover, the lack of correlation between portal pressure and
histological findings should be described in the results section and not in the
discussion.
The paper would improve if the authors transform the semi-quantitative data of
HV Doppler flow pattern into a more objective and numerical index, such as the
damping index (Kim et al. Liver International 2007)
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Reviewer's report
Title:Intrahepatic blood flow assessment by Doppler ultrasonography:
relationship among hepatic vein, portal vein, hepatic artery and portal pressure
intraoperatively measured in patients with portal hypertension
Version: 2Date:11 January 2011
Reviewer: Annalisa Berzigotti
Reviewer's report:
This paper by Zhang and colleagues was aimed at clarifying the
pathophysiological factors associated with abnormalities in hepatic veins Doppler
pattern in patients with cirrhosis and portal hypertension. In 60 patients requiring
surgery for portal hypertension the authors assess simultaneously this Doppler
parameter and portal pressure as measured directly and invasively; they also
measure portal vein velocity and hepatic artery pulsatility index (HAPI) by
Doppler; non-invasive measurements were also performed in a group of healthy
controls.
The results are consistent with a moderate linear correlation between portal
pressure and flattening of flow in the hepatic veins; similarly, portal vein velocity
decreased and HAPI increased in patients with abnormal hepatic vein flow
pattern. It is concluded that in patients with PHT, monophasic HV waveform
indicates higher portal pressure and that it can be hypothesized that
parenchymal fibrosis and fat infiltration reduce HV compliance being the cause of
the abnormality of Doppler HV waveform.
The paper explores an interesting issue, which has been previously evaluated by
other authors but that is still poorly understood. However, the study has some
major limitations, which are listed below:
1) A main flaw of the study is the lack of data about inferior vena cava pressure
and other parameters related to systemic hemodynamics. Absolute portal
pressure is obviously an indicator of the severity of portal hypertension, but from
a pathophysiological point of view the consequences of portal hypertension
depend on the portal pressure gradient, which is calculated as the difference
between portal pressure and inferior vena cava pressure (Bosch et al. Seminars
Liver Diseases 2006). Therefore, the lack of IVC pressure measurement
decreases the reliability of the results.
2) As the authors acknowledge, right heart catheterization or at least
echocardiography should have been performed to rule-out heart valvular
diseases or other conditions which can directly affect HV Doppler pattern.
Moreover, the assessment of cardiac output, systemic arterial pressure and
systemic vascular resistance would have given data on the presence of
hyperdynamic syndrome, which could also be a determinant of abnormality of HV
Doppler flow.
3) The study population is poorly described (see table 1): data on etiology of
cirrhosis, prevalence and size of gastroesophageal varices, previous episodes of
bleeding from varices, ascites, … should be added to support the hypothesis that
abnormalities in HV Doppler pattern depend principally from portal pressure
increase. Indeed, ascites increases intrabdominal pressure which could flatten
HV Doppler pattern.
4) Design of the study: the study lacks a clear hypothesis, which should be better
defined.
5) Study protocol: both portal pressure and central venous pressure can be
affected by drugs used in general anesthesia; the authors should carefully
comment on the protocol of anesthesia used, specifying if this was the same in
all patients, and in which moment PP and Doppler were performed. Were the
patients ventilated? How was respiration suspended?
6) The results show that flattened HV Doppler flow pattern indicated more severe
portal hypertension; however, all patients had severe portal hypertension since
this was an inclusion criteria, and differences in PP between patients with normal
and abnormal flow were very small (2-3 mmHg); how do the authors suggest to
interpret the finding of abnormal HV Doppler pattern in a patients with known
clinically significant portal hypertension? Did the patients with more flattened HV
Doppler pattern show a different outcome on follow-up (decompensation, death,
bleeding…), so supporting a clinical usefulness of the Doppler finding?
7) Discussion: a referral to “liver stiffness” is made in some sentences. In the
methods and results no mention on direct liver stiffness measurement is made;
was liver stiffness evaluated (transient elastography? ARFI? Other methods?) or
is HAPI used as the only surrogate of liver stiffness? If it is so, the authors should
better clarify the background for the use of Doppler impedance of hepatic artery
as an indicator of liver stiffness.
8) Conclusions: Since no correlation was observed between HV Doppler flow
pattern and histological findings it is difficult to accept the conclusion (see last
lines of the abstract), which should be changed.
Minor comments
Histological findings might be better explained in the results section and not only
in table 1; moreover, the lack of correlation between portal pressure and
histological findings should be described in the results section and not in the
discussion.
The paper would improve if the authors transform the semi-quantitative data of
HV Doppler flow pattern into a more objective and numerical index, such as the
damping index (Kim et al. Liver International 2007)
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Please review this paper.
user
Reviewer's report
Title:Intrahepatic blood flow assessment by Doppler ultrasonography:
relationship among hepatic vein, portal vein, hepatic artery and portal pressure
intraoperatively measured in patients with portal hypertension
Version: 2Date:11 January 2011
Reviewer: Annalisa Berzigotti
Reviewer's report:
This paper by Zhang and colleagues was aimed at clarifying the
pathophysiological factors associated with abnormalities in hepatic veins Doppler
pattern in patients with cirrhosis and portal hypertension. In 60 patients requiring
surgery for portal hypertension the authors assess simultaneously this Doppler
parameter and portal pressure as measured directly and invasively; they also
measure portal vein velocity and hepatic artery pulsatility index (HAPI) by
Doppler; non-invasive measurements were also performed in a group of healthy
controls.
The results are consistent with a moderate linear correlation between portal
pressure and flattening of flow in the hepatic veins; similarly, portal vein velocity
decreased and HAPI increased in patients with abnormal hepatic vein flow
pattern. It is concluded that in patients with PHT, monophasic HV waveform
indicates higher portal pressure and that it can be hypothesized that
parenchymal fibrosis and fat infiltration reduce HV compliance being the cause of
the abnormality of Doppler HV waveform.
The paper explores an interesting issue, which has been previously evaluated by
other authors but that is still poorly understood. However, the study has some
major limitations, which are listed below:
1) A main flaw of the study is the lack of data about inferior vena cava pressure
and other parameters related to systemic hemodynamics. Absolute portal
pressure is obviously an indicator of the severity of portal hypertension, but from
a pathophysiological point of view the consequences of portal hypertension
depend on the portal pressure gradient, which is calculated as the difference
between portal pressure and inferior vena cava pressure (Bosch et al. Seminars
Liver Diseases 2006). Therefore, the lack of IVC pressure measurement
decreases the reliability of the results.
2) As the authors acknowledge, right heart catheterization or at least
echocardiography should have been performed to rule-out heart valvular
diseases or other conditions which can directly affect HV Doppler pattern.
Moreover, the assessment of cardiac output, systemic arterial pressure and
systemic vascular resistance would have given data on the presence of
hyperdynamic syndrome, which could also be a determinant of abnormality of HV
Doppler flow.
3) The study population is poorly described (see table 1): data on etiology of
cirrhosis, prevalence and size of gastroesophageal varices, previous episodes of
bleeding from varices, ascites, … should be added to support the hypothesis that
abnormalities in HV Doppler pattern depend principally from portal pressure
increase. Indeed, ascites increases intrabdominal pressure which could flatten
HV Doppler pattern.
4) Design of the study: the study lacks a clear hypothesis, which should be better
defined.
5) Study protocol: both portal pressure and central venous pressure can be
affected by drugs used in general anesthesia; the authors should carefully
comment on the protocol of anesthesia used, specifying if this was the same in
all patients, and in which moment PP and Doppler were performed. Were the
patients ventilated? How was respiration suspended?
6) The results show that flattened HV Doppler flow pattern indicated more severe
portal hypertension; however, all patients had severe portal hypertension since
this was an inclusion criteria, and differences in PP between patients with normal
and abnormal flow were very small (2-3 mmHg); how do the authors suggest to
interpret the finding of abnormal HV Doppler pattern in a patients with known
clinically significant portal hypertension? Did the patients with more flattened HV
Doppler pattern show a different outcome on follow-up (decompensation, death,
bleeding…), so supporting a clinical usefulness of the Doppler finding?
7) Discussion: a referral to “liver stiffness” is made in some sentences. In the
methods and results no mention on direct liver stiffness measurement is made;
was liver stiffness evaluated (transient elastography? ARFI? Other methods?) or
is HAPI used as the only surrogate of liver stiffness? If it is so, the authors should
better clarify the background for the use of Doppler impedance of hepatic artery
as an indicator of liver stiffness.
8) Conclusions: Since no correlation was observed between HV Doppler flow
pattern and histological findings it is difficult to accept the conclusion (see last
lines of the abstract), which should be changed.
Minor comments
Histological findings might be better explained in the results section and not only
in table 1; moreover, the lack of correlation between portal pressure and
histological findings should be described in the results section and not in the
discussion.
The paper would improve if the authors transform the semi-quantitative data of
HV Doppler flow pattern into a more objective and numerical index, such as the
damping index (Kim et al. Liver International 2007)
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
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