1

Document for the EFSUMB

Education and Professional Standard Committee.

Clinical recommendations for the performance and reporting of

ultrasound examination for portal hypertension

Annalisa Berzigotti1,2

, Fabio Piscaglia3 and the EFSUMB Education and Professional

Standard Committee

1Hepatic Hemodynamic Laboratory, Liver Unit, Institut d'Investigacions Biomediques

August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de

Enfermedades Hepáticas y Digestivas (Ciberehd); 2Abdominal Imaging Section, Centre

Diagnostic per la Imatge (CDIC), Hospital Clinic i Provincial, c/Villarroel 170, 08036,

Barcelona, Spain.

3Division of Internal Medicine, Department of Digestive Disease and Internal Medicine,

General and University Hospital S.Orsola-Malpighi, Bologna, Italy

Address for correspondence:

Annalisa Berzigotti, M.D., Ph.D.,

Abdominal Imaging Section, Centre Diagnostic per la Imatge (CDIC),

Hospital Clinic i Provincial

c/Villarroel 170

08036, Barcelona, Spain

e-mail: aberzigo@clinic.ub.es

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Preface

This document contains clinical recommendations about how to perform and report

ultrasound examinations in patients with suspected or previously diagnosed portal

hypertension. To ensure an updated content, a bibliographic research on studies

involving ultrasound in this specific field was conducted (Medline, last updated in

March 2011).

The document, which is intended as straightforward and concise, has been structured as

follows:

- Introduction containing the essential clinical background of portal hypertension

- Main clinical information derived from US in this field (further commented in

Table 1, Table 2 and Table 4)

- Technical details of US-Doppler examination in this field (further commented

in Table 3)

- EFSUMB endorsed recommendations on how reports of US examinations have

to be arranged. In particular a list of parameters related to presence of clinically

significant portal hypertension (CSPH) which should be included in all US

report according to the level of care of the ultrasound unit in which the patients

is investigated (primary, secondary or tertiary referral center; Table 4 and 5)

All the contents are expanded and discussed in a free access CME-article to be

published in Ultraschall in der Medizin-European Journal of Ultrasound, which also

contains US images to illustrate the most important aspects of duplex-US

assessment in portal hypertension.

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Introduction

Portal hypertension (PH) is a frequent clinical syndrome hemodynamically defined

by an increase in the portal pressure gradient (difference between portal vein

pressure and inferior vena cava pressure) over the normal limit of 5 mmHg (1). The

clinical features of this syndrome include gastroesophageal varices formation and

rupture, ascites and hepato-renal syndrome, which are the main causes of death and

liver transplantation in patients with cirrhosis.

In Western countries 90% of cases of PH are due to liver cirrhosis, which is its main

intrahepatic cause, while rarer etiologies include pre-hepatic causes such as portal

vein thrombosis (more common in children), and post-hepatic causes, such as

hepatic veins thrombosis (Table 1).

In parenchymal chronic liver diseases PH begins to develop as a consequence of the

architectural disarrangement induced by scarring and nodules, which induce an

increased resistance to blood inflow. In later phases, when PH is already established,

it is maintained by splanchnic vasodilatation and formation of porto-systemic

collaterals which induce an increase in porto-collateral blood flow (for similarity

and generalization of Ohm’s law: Voltage = Resistance by Current, in

hemodynamics it can be considered Pressure=Resistance * Flow) (1).

The gold standard for PH assessment in cirrhosis is the invasive measurement of

hepatic venous pressure gradient (difference between wedged hepatic venous

pressure and free hepatic venous pressure, HVPG) by means of hepatic vein

catheterization. HVPG over 10-12 mmHg defines clinically significant portal

hypertension (CSPH), since all complications can occur when pressure increases

above this threshold (1).

The development of clinically significant portal hypertension (CSPH, HVPG ≥ 10

mmHg) is a key prognostic step in the natural history of cirrhosis; even in patients

with compensated cirrhosis and no gastroesophageal varices, the presence of CSPH

is an independent predictor of clinical decompensation (namely: ascites, variceal

bleeding, hepatic encephalopathy, jaundice, hepato-renal syndrome, spontaneous

bacterial peritonitis) and death (2). Therefore, in patients with chronic liver diseases

CSPH should be diagnosed promptly to allow accurate risk stratification and to

provide appropriate clinical management, including endoscopy screening for

esophageal varices and pharmacological treatment when indicated. Even if HVPG

gives irreplaceable information, it is invasive, relatively expensive in terms of

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disposable and need for angiography room occupancy and its use is currently

restricted to tertiary care hospitals.

Ultrasound (US) is the first line imaging technique used in patients with suspected

PH, since it is non-invasive, repeatable and cheap. Therefore, all US examiners

should be able to detect and report correctly the most important signs of PH.

Most US signs of PH are independent of its underlying cause, and their

interpretation should always be integrated with clinical information. On the other

hand, when patients show overt clinical features of PH and no other data is

available, US examination facilitates the classification of PH.

These recommendations are intended as a guide for standardizing and ensuring a

high-quality examination and reporting of US in patients with suspected/established

portal hypertension.

Clinical scenario, indications and main information derived from US in this

field

There are four main clinical scenarios of application of US in the field of portal

hypertension:

1. Patients with clinical/laboratory findings of PH in the absence of known chronic

liver disease (CLD)

The chance of encountering non-cirrhotic causes of PH is increased in these

patients, and special attention should be paid in the assessment of vascular patency,

since portal vein thrombosis and hepatic veins thrombosis are the most frequent

causes of non-cirrhotic portal hypertension.

Colour (and Power)-Doppler US (CDUS) is > 90% accurate for diagnosing portal

vein thrombosis/portal cavernoma and hepatic veins thrombosis (Budd-Chiari

syndrome); cardiac causes, and arterioportal fistulae can be also identified. Rarer

causes of PH (including idiopathic portal hypertension or nodular regenerative

hyperplasia) should be suspected in patients with signs of PH and no other apparent

cause, and should be investigated with appropriate invasive means.

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2. US assessment of PH in patients with known compensated chronic liver disease

(CLD)

Up to 70% of patients with compensated cirrhosis have CSPH (defined as

HVPG10 mmHg). Therefore, signs of cirrhosis should be always investigated; the

most accurate single sign of cirrhosis is liver surface nodularity examined by a

linear transducer (1, 3, 4).

Table 2 shows the most important US signs of PH. US signs are highly specific for

the non-invasive diagnosis of CSPH, but their sensitivity is moderate.

The fundamental signs are:

- Porto-systemic abdominal collaterals

- Splenomegaly

- Portal vein, splenic vein and mesenteric vein dilatation

- Reduction of the respiratory variations of splenic and mesenteric vein diameter

- Hepatofugal flow in the portal vein system

- Reduction of portal vein blood velocity

- Subclinical ascites

Ancillary US parameters of PH are the congestion index of the portal vein (5);

flattening of physiologic phasicity of hepatic veins Doppler flow pattern (6, 7) and

arterial parameters (renal Doppler impedance indexes, splenic artery Doppler

impedance indexes and superior mesenteric artery Doppler impedance indexes) (8,

9).

Even if the signs listed above, especially when combined, can reliably diagnose

CSPH, none of them allows an exact numerical estimation of the HVPG.

Portal vein thrombosis and/or to hepatocellular carcinoma can cause abrupt

increases in portal pressure leading to episodes of clinical decompensation.

RECOMMENDATION

In patients with clear clinical signs of portal hypertension duplex-Doppler US is

an accurate method to establish the causes of portal hypertension.

Specifically, portal vein thrombosis and hepatic vein thrombosis can be

identified or ruled-out by duplex-Doppler US

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Therefore, anytime new clinical events occur, patients should be re-assessed by US-

Doppler to rule-out these complications.

3. Prognostic information provided by US findings in patients with cirrhosis and PH

Porto-systemic collaterals are associated with an increased prevalence of

esopheageal varices, with a higher risk of first clinical decompensation of cirrhosis

(10), and with the onset of hepatocellular carcinoma (11).

The development/increase in number of porto-systemic collaterals, and spleen

enlargement on follow-up have been associated with a greater proportion of variceal

formation and growth (12, 13). Increased congestion index of the portal vein

RECOMMENDATION

All patients with chronic liver diseases should undergo a US-Doppler

examination at the time of first diagnosis to assess the presence of signs of

cirrhosis and portal hypertension, since US signs hold a satisfactory sensitivity

and a high specificity for the diagnosis of these conditions.

The essential parameters to be described are: signs of cirrhosis; portal vein

patency, diameter and direction of flow; splenic vein and mesenteric vein

diameter and its respiratory variation, and direction of flow, spleen size,

presence/absence of porto-systemic abdominal collaterals and presence/absence

of ascites.

Most US-Doppler signs show high specificity for the diagnosis of CSPH. Since

US-Doppler is non-invasive and repeatable, the search of these specific findings

according to the level of care reported in Table 3 is recommended.

In patients with cirrhosis US-Doppler examination should be repeated every

time a new clinical event occurs, to rule out portal vein thrombosis and

hepatocellular carcinoma, which are frequent causes of worsening of portal

hypertension and clinical decompensation.

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independently predicted first variceal bleeding in the following 6 months (but not on

the long-term) in one study (14).

A slow portal vein flow (averaged maximum velocity <15 cm/s) was the only

variable independently associated with a higher risk of developing non-malignant

(bland) portal vein thrombosis in a recent prospective study in cirrhotic patients

(15).

Increased intrarenal arteriolar Doppler RI (RI ≥0.70) indicates downstream arterial

vasoconstriction and is a useful sign contributing to diagnosing hepato-renal

syndrome (16, 17).

A small liver size, spleen size over 14.5 cm, mean portal vein velocity < 10 cm/s

and loss of pulsatility of hepatic veins have all been associated to higher mortality

on follow-up in patients with compensated cirrhosis.

A more detailed discussion of these parameters can be found in the CME-article.

4. Follow-up of patients receiving treatment for portal hypertension

Treatment aiming at decreasing portal pressure are a) pharmacological treatment,

mainly consisting in betablockers or betablockers plus nitrates, b) surgical porto-

systemic shunts and c) transjugular intrahepatic portosystemic shuns (TIPS).

Doppler ultrasound has an established clinical role in the assessment of the two

latter situations (see Table 3), whereas its usefulness in the former is uncertain.

Technical details: how to conduct US and Doppler US examinations of the

liver, spleen and portal venous system (Table 3).

US and Doppler-US examination should be performed after at least 6 hour fast, by

using real-time scanners provided with pulsed and colour/power Doppler modules

(convex transducers; mean frequencies used are between 3.5 and 5 MHz; linear

high-frequency transducers 7.5-10 MHz are useful to assess liver surface).

RECOMMENDATION

Doppler-US does not provide accurate information on the hemodynamic

response to beta-blockers in patients with cirrhosis and portal hypertension.

Doppler-US is useful and recommended to non-invasively follow-up patients

with TIPS or porto-systemic surgical shunts.

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For Doppler parameters at least three consistent consecutive measurements should

be taken, and their average used as the final result. Note that the normal values

described in the table have been set according to the data of published studies,

which are mostly case series or case-control studies; randomized controlled trials in

this field are lacking, and better evidence cannot be provided.

List of parameters related to presence of CSPH which should be included in all

US report grouped according to the level of care of the ultrasound unit in

which the patients is investigated (primary, secondary or tertiary referral

center)

Table 4 and Table 5 summarize the information which should be given in US

reports according to the level of care of the referral center. A list of parameters

which should be intended for research use and not for clinical practice is also

provided.

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Table 1. Causes of portal hypertension according to the site of increased resistance to

portal blood flow, and usefulness of US and Doppler-US for diagnosis.

Site of increased resistance to

portal blood flow Main causes

Ultrasound usefulness for

specific diagnosis

Presinusoidal

Prehepatic

• Thrombosis of the portal system

• Congenital stenosis of the portal

vein

• Arteriovenous fistulae (splenic,

aortomesenteric, aortoportal, and

hepatic artery-portal vein)

Yes:

Lack of patency or abnormal

morphology of portal vein

system; visualization of

fistulae or of their

hemodynamic consequences

Intrahepatic

• Partial nodular transformation

• Nodular regenerative hyperplasia

• Congenital hepatic fibrosis

• Peliosis hepatis

• Polycystic liver disease

• Schistosomiasis

• Idiopathic portal hypertension

• Hypervitaminosis A

• Arsenic, copper sulfate, and vinyl

chloride monomer poisoning

• Sarcoidosis

• Tuberculosis

• • Amyloidosis

• Acute fatty liver of pregnancy

Only in some cases (underlined in the causes

column):

Multiple hepatic cysts

Wall thickening and

increased echogenicity of

the portal veins and its

branches; anechoic portal

vein surrounded by

echogenic fibrous tissue

configuring the typical

“bull’s eye” (18)

In the remaining: non-

specific liver alterations

Sinusoidal

• Liver cirrhosis

(alcoholic, viral, etc...)

• Sinusoidal obstruction syndrome

(SOS)* also known as veno-

occlusive disease

Yes

In cirrhosis: liver surface

irregularity and changes of

liver morphology

In SOS: hepatomegaly,

ascites, gallbladder wall

thickening and decreased or

reversed portal venous

flow(19)

Postsinusoidal

Intrahepatic

• Budd-Chiari syndrome

Yes

Lack of patency of hepatic

veins

Posthepatic

• Congenital malformations and

thrombosis of the IVC

• Constrictive pericarditis

• Tricuspid valve diseases

Yes

Lack of patency of IVC

Dilatation and abnormal

flow pattern of hepatic veins

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Table 2. Main reported US and Doppler-US signs of portal hypertension in patients

with chronic liver diseases. Accuracy in populations including patients with other

relevant comorbidity (cardiac disease, haematologic diseases) is unknown. *Gold

standard for PH diagnosis: HVPG measurement or direct measurement; sensitivity efers

to patients with HVPG 12 mmHg.

Refs

Sensitivity

Specificity

Portal

venous

system

Dilatation of portal vein (13 mm)

(20, 21) <50% 90-100%

Dilatation of splenic vein (SV) and

superior mesenteric vein (SMV) (11 mm)

(22, 23) 72% 100%

Reduction of portal vein blood flow

velocity (Time Averaged Max Vel < 16

cm/s; mean vel < 10 cm/ s)

(24, 25) 80-88% 80-96%

Reversal of portal vein blood flow (26) Not reported;

sign prevalence:

8.3% of

unselected pts

100%

Increased portal vein congestion index

(0.08)

(5, 25)* 67-95% 100%

Reduction of respiratory variation of

diameter in SV or SMV (<40%)

(20) 79.7% 100%

Spleen Splenomegaly (diameter > 12 cm and/or

area 45 cm2)

(27)* 93% 36%

Splenic

artery

Increased Doppler impedance indexes in

the intraparenchymal branches (RI ≥0.63,

PI≥1.00)

(28)*(29,

30) 84.6% 70.4%

Hepatic

artery

Increased Doppler resistive index in the

intrahepatic branches (>0.78)

(30, 31) 50% 100%

Renal

artery

Increased Doppler resistive index of the

right interlobar renal artery ( 0.65)

(28)* 79.5% 59.3%

SMA Decreased Doppler pulsatility index (

2.70)

(28)* 85.7% 65.2%

Presence of porto-systemic collateral circulation (32)* 83% 100%

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Table 3. Technical details of US examination for portal hypertension.

Where to measure How to measure and normal values

Portal

vein (PV)

Diameter

Oblique-transversal

scan in

epigastrium/right

subcostal region to

visualize PV along its

longitudinal axis for at

least 3-4 cm

- Measure PV diameter as distance from inner anterior wall to inner posterior

wall, perpendicular to the long portal axis, at the cross with hepatic artery or

slightly downstream (but ≥2 cm upstream from portal bifurcation) wherever the

vessel walls are best visualized: aim to a large angle between US waves and

portal walls.

- Diameter is to be preferably measured with grey scale B-mode ultrasound,

since CDUS, despite facilitating identification of the vessel, also implies a risk of

overestimation of diameter, related to the size of the color pixels.

- Measured during normal suspended respiration in the supine position (forced

inspiration or left side decubitus make measurement unreliable)

- Normal < 12 mm (diameter increases according to body surface)

Velocity

- Place sample volume (≥50% of the diameter of PV) in the middle of the lumen

at the cross with hepatic artery (33)

- Doppler angle preferably set at 55°, but keep it always 60º

- Doppler flowmetry, recommended PRF=4 kHz; wall filter=100 Hz (decrease to

50 Hz if very slow flow)

- concurrent display of colour-Doppler image and Doppler flowmetry

measurement if feasible (top equipments) or freeze B-mode image while

displaying Doppler flowmetry tracings

- Manual tracing of Doppler signal for at least 2 cardiac cycles or ≥2-3 seconds;

mean maximum velocity is calculated by the equipment in cm/s; mean velocity

can be approximated as time averaged max vel*0.57. Direct measurement of

mean portal vein velocity is technically feasible but strongly influenced by

Doppler setting, resulting in low reproducibility. Measurement of time averaged

maximal velocity is recommended

- Normal time averaged maximum vel > 20-24cm/s$

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Congestion index Calculated as PV cross sectional area (diameter/2*diameter/2*) / mean portal

flow velocity

Normal < 0.075

Splenic

vein Diameter

Transversal scan in

epigastrium, to

visualize SV

longitudinal axis

Measure SV diameter at about 1-2 cm upstream the spleno-portal confluence,

during suspended normal respiration in supine position

Diameter ≥ 10 mm is to be considered enlarged

Superior

mes. vein Diameter

Longitudinal scan in

epigastrium, to

visualize SMV

longitudinal axis

Measure SMV diameter at about 1-2 cm upstream the mesenteric-portal

confluence, during suspended normal respiration in supine position

Diameter ≥ 10 mm is to be considered enlarged

Porto-

collateral

circulation

Presence or

absence

At least the following vessels should be actively looked for by US and color-Doppler US:

Paraumbilical vein: falciform ligament

Left gastric vein: epigastric region posterior to left hepatic lobe. Check also flow direction.

Short gastric veins: left hypcondrium posterior to the upper pole of the spleen

Spleno-renal circulation: left hypocondrium between the lower half of the spleen and the left kidney

Hepatic

veins

Diameter and

patency

Right subcostal or right

intercostal scan (the

latter especially for

Doppler flow tracing

Normal diameter ≤ 1 cm

13

Phasicity of flow

measurement) allowing

a main axis

visualization

Sampling at 1-3 cm

from IVC

Sample volume should be about the same as diameter of the vein; quantitative

information (flow velocity) is restricted to selected cases (stenosis)

Normal triphasic flow. Flow tracings to be assessed during suspended normal

respiration (forced inspiration may flatten the tracing, however, if regularly

triphasic during forced inspiration a normal tracing is anyway ascertained).

Assessment at best in supine position, but in left decubitus also acceptable.

Inferior

vena cava

Diameter and

patency

Transversal/longitudina

l scans from the

thoraco-abdominal

region (intercostal and

subcostal)

Normal tri-quadriphasic flow; tend to collaps in expiration. Caliber <2 cm.

Hepatic

artery

Intraparenchymal

Impedance indexes

Main lobar branches in

the right and left lobe

Color-Doppler helps in finding the site of measurement, adjacent to the lobar

branches of the portal vein. Right branch visualized usually at best through an

intercostal scan at its entrance in the liver, left branch through an epigastric scan,

either during suspended normal respiration or during forced inspiration (to be

kept no longer than approximately 10 seconds, otherwise hypoxia induces

vasodilatation). Increase PRF to improve Doppler tracings, aiming at having a

trace occupying approximately ¾ of the screen height. At least 2 identical

consecutive complete arterial tracings are required (at best ≥3) to confirm that no

change in pulsed Doppler insonation angle occurred during the recording of

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tracings in any cardiac cycle.

Normal: RI < 0.65-0.70; PI <1.20

Splenic

artery

Intraparenchymal

Impedance indexes

Main branches 1 cm

after entering the

parenchyma

Color-Doppler helps in finding the site of measurement, usually parallel to the

intrasplenic veins. Adjust PRF to improve Doppler tracings, aiming at having a

trace occupying approximately ¾ of the screen height, after having lowered the

zero Doppler line. Angle of insonation preferable between 20° and 60°.

Measurements through a left intercostal space in the supine position during either

suspended normal respiration or forced inspiration (to be kept no longer than

approximately 10 seconds, otherwise hypoxia induces vasodilation). Sample

volume usually 2-4 mm, often larger than arterial diameter. At least 2 identical

complete arterial tracings are required (at best ≥3) to confirm that no change in

pulsed Doppler insonation angle occurred during the tracing of any cardiac cycle.

Normal: RI < 0.63; PI <1.00

Superior

mesenteric

artery

Diameter and

impedance indexes

Longitudinal scan in

epigastrium, to

visualize SMA

longitudinal axis

Site of assessment. 3-5 cm distal to the origin, at best shortly after the initial

curve, where the course is straight. Sample volume set as large as the artery.

Adjust PRF to improve Doppler tracings, aiming at having a trace occupying

approximately ¾ of the screen height. Normal in fasting state: RI > 0.84; PI

>3.20. Diameter ≤6 mm. At least 2 identical consecutive complete arterial

tracings are required (at best ≥3) to confirm that no change in pulsed Doppler

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insonation angle occurred during the tracing of any cardiac cycle.

Renal

arteries

Intraparenchymal

Impedance indexes

Interlobar (or

interlobular) arteries

Visualize the kidney as superficial as possible (usually through a rather posterior

approach). Preliminary CDUS is strongly recommended to visualize the arterial

tree. Keep CDUS PRF low (700-800 Hz). Measurements taken either during

suspended normal respiration or forced inspiration (to be kept no longer than

approximately 10 seconds, otherwise hypoxia induces vasodilation). Sample

volume usually 2-4 mm, larger than artery diameter. Adjust PRF to improve

Doppler tracings, aiming at having a trace occupying approximately ¾ of the

screen height, after having lowered the zero Doppler line. At least 2 identical

consecutive complete arterial tracings are required (at best ≥3) to confirm that no

change in pulsed Doppler insonation angle occurred during the tracing of any

cardiac cycle.

Normal: RI <0.70 (in adult patients); PI <1.15-1.20

TIPS Patency

Intercostal scan

allowing TIPS

visualization from the

portal vein up to the

- Assess TIPS patency (presence of flow) by colour-Doppler

- Assess flow velocity within TIPS (proximal, medium and distal part); a focal

increase in velocity suggests TIPS dysfunction/stenosis

- Evaluate the direction of flow within the intrahepatic branches of portal vein;

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hepatic vein hepatofugal (reversed) flow is associated with normal TIPS function, while the

re-appearance of hepatopetal flow (if previously reversed) in the follow-up is

associated with TIPS dysfunction

- Measure portal vein velocity: a progressive reduction in subsequent controls

suggests TIPS dysfunction

- Presence of ascites is highly suggestive of TIPS dysfunction

Surgical

shunts Patency

Transverse and

longitudinal scan in the

anatomical site

according to the type of

shunt (spleno-renal

shunt; porto-caval

shunt; meso-cava

shunt)

B-mode and Colour Doppler examination if possible; if not feasible due to

abdominal gas evaluate indirect signs of patency: absence of ascites and reversal

of flow in the portal vein (porto- and meso-cava shunt) or in the splenic vein

(proximal spleno-renal shunt) suggest patency

$ Normality range should be assessed for every US equipment, since interequipment variability is large.

17

Table 4. Information to be included in all US reports of any patient with a request to investigate presence of portal hypertension or any

patient in whom chronic liver disease or ascites of unknown origin is diagnosed, subgrouped according to the level of care of the ultrasound

unit providing the examination.

US/ US-Doppler Parameter

Primary

referral

center

Secondary

referral

center

Tertiary

referral

center

Intended for research use

and not for clinical

practice

Presence/absence of signs of cirrhosis (at least the

pattern of liver surface, preferentially with a linear

probe, and liver echotexture) and focal lesions in the

liver

X X X

Patency of hepatic veins (HV) X X X

Course (linearity) and diameter of HV (semiquantitative:

decreased, normal or increased)

X

X

Morphology of HV Doppler flow X X

In case of Budd-Chiari syndrome: assessment of the

presence of intrahepatic collateral circulation and

enlargement of short hepatic veins in the caudate lobe;

use of contrast agents to confirm the diagnosis

X

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Patency and diameter of portal vein X X X

Patency of intrahepatic main and segmental branches of

portal vein

X X

Direction of flow into the portal vein X X X

Portal vein flow velocity X X

In case of thrombosis: assess whether it is partial or

total; if partial thrombosis state, approximately, the

percent of lumen occupied by thrombosis

X X

Use of CDUS + CEUS with contrast agents to confirm

the diagnosis of portal thrombosis in difficult cases and

to characterize the thrombus (benign vs. malignant

thrombus)

X

Portal blood flow volume X

Patency, diameter and flow direction in splenic vein and

superior mesenteric vein

X X

Assessment of respiratory variation of the diameter of

splenic vein and superior mesenteric vein

X X

Spleen size (longitudinal diameter and/or cross sectional

area)

X X X

Presence or absence of portosystemic collateral vessels X X X

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(if present, location is to be reported)

Presence or absence of ascites X X X

Semi-quantitative assessment of the amount of ascites

(minimal, mild, moderate, massive)

X X

Diameter of main hepatic artery; hepatic artery velocity X

Intrahepatic artery Doppler pulsatility and resistance

index (right and left lobe)

X

Hepatic artery blood flow X

Total hepatic blood flow X

Diameter of splenic artery; splenic artery velocity X

Diameter of superior mesenteric artery; SMA velocity X

Intraparenchymal splenic artery Doppler pulsatility and

resistance indexes

X

Intraparenchymal renal (interlobar artery) Doppler

pulsatility and resistance indexes

X

Superior mesenteric artery Doppler pulsatility and

resistance indexes

X

Liver vascular index (34) X

Portal hypertension index (30) X

20

Porto-hepatic transit time of contrast medium by CEUS

(35)

X

Regional hepatic perfusion by CEUS (36) X

21

Table 5. Summary of parameters to be reported according to the level of the Ultrasound Unit, and clinical correlates. Recommendation

endorsed by the EFSUMB Education and Professional Standard Committee.

Level of US

examination Parameters to be assessed Clinical correlates of the US and Doppler US findings

Primary

level

Signs of cirrhosis (liver profiles, hepatic morphology

changes and echotexture); focal liver lesions; patency

and diameter of hepatic veins; patency, diameter and

flow direction of the portal vein; presence of ascites;

presence of portal systemic collaterals; spleen size

1) Porto-systemic collaterals are pathognomonic features of Clinically

Significant Portal Hypertension (CSPH), regardless of the presence of

cirrhosis, suggests the presence of gastroesophageal varices and has

been associated with a higher risk of first clinical decompensation of

cirrhosis; development/increase in number of porto-systemic collaterals

has been associated with a greater proportion of variceal formation and

growth

2) Portal vein thrombosis is diagnostic of portal hypertension (in the

absence of cirrhosis its etiologic assessment requires specific

investigations).

3) Reversal of flow within any main vessel of portal system is diagnostic

of portal hypertension

4) Splenomegaly, ascites and portal vein dilation are all highly

suggestive of CSPH only in patients with cirrhosis; in the absence of

cirrhosis and hepatic/portal veins obstruction other causes are to be

intensively seeked for.

5) Increased spleen size is predictive of mortality in cirrhosis, and spleen

enlargement on follow-up has been associated with a greater proportion

22

of variceal formation and growth, and with a higher risk of first clinical

decompensation of cirrhosis

5) Obstruction of hepatic veins in the absence of liver tumors is

pathognomonic of Budd-Chiari syndrome (whose etiologic assessment

requires specific investigations).

6) Enlargement of the hepatic veins (and inferior vena cava) suggests a

post-hepatic cause of CSPH (cardiac liver).

7) A small liver size is associated with mortality in cirrhosis

Secondary

level

All parameters of primary level plus: course,

diameter and flow Doppler tracing in hepatic veins;

patency and flow direction in the intrahepatic portal

branches and in splenic and superior mesenteric

veins; portal vein flow velocity; portal vein thrombus

extension; assessment of respiratory variations of

caliber in the splenic and superior mesenteric veins.

All the above, plus:

1) Reversal of flow in the right portal vein or in the splenic or superior

mesenteric veins are diagnostic of CSPH

2) Increased congestion index of the portal vein independently predicted

6-moths risk of first variceal bleeding

3) Decrease in portal vein flow velocity contributes to the diagnosis of

cirrhosis in compensated chronic liver disease; severe decrease in portal

vein flow velocity indicates CSPH, is a negative prognostic factor in

compensated cirrhosis, and might predict the risk of non-malignant

portal vein thrombosis

4) Ridigity (absence of respiratory variations) of splenic and superior

mesenteric veins is highly suggestive for portal hypertension

5) Presence of portal vein thrombosis, even if partial and not involving

the portal trunk (splenic vein or superior mesenteric vein, and lobar

23

intrahepatic branches), is pathognomonic of portal hypertension

6) flattening of hepatic vein flow tracing occurs in chronic liver disease;

when occurring in cirrhosis has a negative prognostic value

Tertiary

(referral)

level

All parameters of primary and secondary levels plus:

splenic and renal arteries; characterization and study

of extension of portal vein thrombosis; thorough

assessment of hepatic veins.

All the above, plus:

1) increase in splenic artery impedance indexes is highly suggestive of

CSPH in patients with cirrhosis

2) increase in renal artery impedances indexes is an independent

predictor of hepato-renal syndrome

3) distinction between bland and malignant portal vein thrombosis

4) complete overview of the vascular situation in patients with Budd-

Chiari syndrome, including thorough assessment of hemodynamics.

5) Diagnosis of non-cirrhotic causes of portal hypertension (fistulae,

cardiac causes, etc.)

24

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