Assessing Portal Hypertension in Liver Diseases

Expert Review of Gastroenterology & Hepatology
ISSN: 1747-4124 (Print) 1747-4132 (Online) Journal homepage: https://www.tandfonline.com/loi/ierh20
Assessing portal hypertension in liver diseases
Annalisa Berzigotti, Susana Seijo, Enric Reverter & Jaime Bosch
To cite this article: Annalisa Berzigotti, Susana Seijo, Enric Reverter & Jaime Bosch (2013)
Assessing portal hypertension in liver diseases, Expert Review of Gastroenterology &
Hepatology, 7:2, 141-155, DOI: 10.1586/egh.12.83
To link to this article: https://doi.org/10.1586/egh.12.83
Published online: 10 Jan 2014.
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Assessing portal hypertension

in liver diseases
Expert Rev. Gastroenterol. Hepatol. 7(2), 141–155 (2013)
Annalisa Berzigotti1,2, Portal hypertension is a common complication of chronic liver diseases and is responsible for most
Susana Seijo1,2, clinical consequences of cirrhosis, which represent the more frequent causes of death and liver
Enric Reverter1,2 and transplantation in these patients. This review is aimed at clarifying the state-of-the art assessment
of portal hypertension and at discussing recent developments in this field. Particular attention is
Jaime Bosch*1,2
paid to new noninvasive techniques that will be soon available for potential routine use.
1
Hepatic Hemodynamic Laboratory,
Liver Unit, Hospital Clinic – Institut
d’Investigacions Biomediques August
Pi i Sunyer (IDIBAPS), University of Keywords: hepatic hemodynamics • hepatic venous pressure gradient • liver stiffness • noninvasive methods
Barcelona, Spain • ultrasound
2
Centro de Investigación Biomédica
en Red de Enfermedades Hepáticas y
Digestivas (CIBERehd), Hospital Clínic,
c/Villarroel 170, 08036 Barcelona, Spain
*Author for correspondence:
Tel.: +34 932 275 790
Medscape: Continuing Medical Education Online
jbosch@clinic.ub.es
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Learning objectives
Upon completion of this activity, participants will be able to:
• Analyze the initial evaluation of a patient with suspected portal hypertension
• Assess testing for gastroesophageal varices among patients with portal hypertension
• Evaluate patterns of portal hypertension on measurement of the hepatic venous pressure gradient
• Distinguish clinically significant elevations in the hepatic venous pressure gradient
www.expert-reviews.com 10.1586/EGH.12.83 © 2013 Expert Reviews Ltd ISSN 1747-4124 141

Review Berzigotti, Seijo, Reverter & Bosch CME
Financial & competing interests disclosure

Editor
Elisa Manzotti
Publisher, Future Science Group, London, UK
Disclosure: Elisa Manzotti has disclosed no relevant financial relationships.
CME Author
Charles Vega
Health Sciences Clinical Professor; Residency Director, Department of Family Medicine, University of California, Irvine, CA, USA
Disclosure: Charles P Vega, MD, has disclosed no relevant financial relationships.
Authors and Credentials
Annalisa Berzigotti, MD, PhD
Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic-Institut d’Investigacions Biomediques August Pi i Sunyer (IDIBAPS), University of
Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Spain
Disclosure: Annalisa Berzigotti, MD, PhD, has disclosed no relevant financial relationships.
Susana Seijo, MD
Disclosure: Susana Seijo, MD, has disclosed no relevant financial relationships.
Enric Reverter, MD
Disclosure: Enric Reverter, MD, has disclosed no relevant financial relationships.
Jaime Bosch, MD, PhD, Professor of Medicine; Chief, Hepatology Section
Disclosure: Jaime Bosch, MD, PhD, has disclosed no relevant financial relationships.
Definition Portal hypertension is an almost unavoidable consequence

Portal hypertension is a frequent syndrome – most often caused by of cirrhosis [1] . Between 80 and 90% of totally asymptomatic
chronic liver diseases – which is characterized by an increased por- patients already have an elevated PPG (measured clinically as an
tal pressure gradient (PPG; the difference in pressure between the increase in the hepatic venous pressure gradient [HVPG]) and
portal vein and the inferior vena cava [IVC], which represents the endoscopy discloses that 40% already have esophageal varices.
perfusion pressure of the liver with portal blood). The increased Among those without varices, this will appear at a rate of 6% per
portal pressure leads to other consequences, such as splenomegaly, year (over 10% in those with a HVPG >10 mmHg). If untreated,
growth of an extensive network of portal-systemic collaterals that bleeding occurs within 2 years in 10–30% of patients with varices,
shunt portal blood flow to the systemic circulation bypassing depending on the size of varices, presence of red color signs,
the liver and development of a hyperkinetic circulatory state [1] . degree of liver failure and of HVPG elevation. Variceal bleeding
In normal conditions the PPG ranges between 1 and 5 mmHg. is associated with a 6-week mortality of 12–20% and if no effec-
Portal hypertension becomes clinically significant (associated tive therapy is provided will recur in two-thirds of the patients
with risk of clinical complications) when the PPG increases to within 2 years. Current medical treatment decreases the risk of
10 mmHg or above. Values between 5 and 9 mmHg represent first and/or recurrent variceal bleeding by approximately 50%,
subclinical portal hypertension [1–3] . indicating that b etter treatments are required.
Natural history Pathophysiology

The relevance of portal hypertension derives from the frequency Portal hypertension is initiated by an increased resistance to por-
and severity of its complications, which represent the first cause tal blood flow and aggravated by an increased portal-collateral
of hospital admission, death and liver transplantation in patients blood flow [4] . Such increased resistance to portal blood flow
with cirrhosis. These include formation of esophageal or gastric is most commonly due to chronic liver disease (cirrhosis of the
varices, variceal bleeding, ascites, spontaneous bacterial peri- liver), which is the most common cause of portal hypertension
tonitis, hepatorenal syndrome, portopulmonary hypertension, worldwide, followed by hepatic schistosomiasis. Other causes of
hepatopulmonary syndrome, hepatic encephalopathy, portal portal hypertension account for less than 10% of cases; among
hypertensive gastropathy (PHG), enteropathy and colopathy these relatively uncommon causes the more frequent are extra-
and disturbances in the metabolism of endo- and xeno-biotics hepatic portal vein occlusion and ‘idiopathic’ noncirrhotic portal
normally metabolized by the liver. hypertension.
142 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

CME Assessing portal hypertension in liver diseases Review
Hepatic vascular resistance in cirrhosis increases by a dual mech- and the right atrium) may cause portal hypertension. Therefore,
anism; first there is a structural component, related to distortion of causes of portal hypertension can be classified according to their ana-
liver microcirculation by fibrosis, nodule formation, angiogenesis tomical location in: prehepatic (involving the spleno–portal–mes-
and vascular occlusion. In addition, there is an increased hepatic enteric venous axis), intrahepatic and posthepatic, as summarized
vascular tone (dynamic component), owing to the contraction in Figure 1 [1,6] . Cirrhosis is the most common cause of portal hyper-
of activated hepatic stellate cells and myofibroblasts around the tension in western countries. All other causes included in so-called
hepatic sinusoids and in fibrous septa and of vascular smooth ‘noncirrhotic portal hypertension’, account for less than 10% of the
muscle cells in the hepatic vasculature. This dynamic compo- cases. In other geographical areas schistosomiasis (Africa) and portal
nent accounts for approximately 30% of the increased hepatic vein thrombosis (India) are leading causes of portal hypertension.
resistance in cirrhosis and represents a liver
vascular dysfunction, with increased local
production of vasoconstrictors (endothe-
lins, angiotensin-II, norepinephrine and
thromboxane A2) and reduced release
of endothelial vasodilators (mainly nitric
oxide, but also carbon monoxide) [4] .
In advanced stages increased splanchnic Constrictive
Posthepatic PH pericarditis
(portal-collateral) blood flow plays a major Tricuspid valve
role maintaining and aggravating portal Increased FHVP; HVPG
normal or slightly diseases
hypertension. It is caused by a marked increased Budd–Chiari syndrome
splanchnic arteriolar vasodilation and neo-
• Congenital malformations
angiogenesis in response to an increased and thrombosis of the IVC
release of VEGF, nitric oxide and other
splanchnic vasodilators. Splanchnic vasodil-
atation is so marked as to determine systemic Intrahepatic PH
hypotension, vascular underfilling, stimu-
lation of endogenous vasoactive systems, Liver cirrhosis
Severe acute hepatitis (viral and alcoholic),
plasma volume expansion and increased Sinusoidal chronic active hepatitis, mastocytosis, Gaucher’s
cardiac index (hyperkinetic syndrome), Increased HVPG due disease, vascular maligancies, amyloidosis, acute fatty
which plays a key role in the pathogenesis to increased WHVP liver of pregnancy, hypervitamin A; SOS (previously VOD)
of ascites and renal dysfunction in cirrho-
sis. Formation of portal–systemic collaterals Schistosomiasis
and varices is not only due to increased por- Nodular regenerative hyperplasia, partial nodular
tal pressure causing opening of pre-existent transformation, congenital hepatic fibrosis
Presinusoidal Idiopathic portal hypertension
vessels at sites of communication between Normal or slightly Peliosis hepatis, polycystic liver disease, arsenic,
the portal and systemic circulation, but is increased HVPG copper sulfate and vinyl chloride monomer
also dependent on angiogenesis [5] . These poisoning, sarcoidosis, tuberculosis,
disturbances provide a rational basis for the primary biliary cirrhosis,
treatment of portal hypertension and are amyloidosis
being used as therapeutic targets [4] .
The abovementioned considerations
Portal vein thrombosis
highlight the importance of an early rec- Splenic and mesenteric
ognition and precise diagnosis of portal vein thrombosis
hypertension for a correct management of Arteriovenous fistulae
patients with chronic liver diseases. This Prehepatic PH Congenital stenosis of PV
Normal HVPG Extrinsic compression of the
requires the use of a number of techniques Normal WHVP and FHVP portosplenic venous axis
that have found increased applicability as
recent studies have shown that they provide
relevant prognostic information. These are
Expert Rev. Gastroenterol. Hepatol. © Future Science Group (2013)
reviewed in this paper.
Figure 1. Classification of portal hypertension based on the site of increased
Etiology & classification of portal resistance and on the hemodynamic findings.
hypertension FHVP: Free hepatic venous pressure; HVPG: Hepatic venous pressure; IVC: Inferior vena
Any disease that may interfere with portal cava; PH: Portal hypertension; PV: Portal vein; SOS: Sinusoidal obstruction syndrome;
blood flow (at any level between the spleen WHVP: Wedge hepatic venous pressure.
www.expert-reviews.com 143
Portal vein thrombosis is the main cause of prehepatic portal The measurement of HVPG is a safe and reproducible tech-
hypertension. In adults, prothrombotic diseases that are either nique that is the preferred way of measuring the PPG in cirrhosis
congenital (such as antithrombin, protein C or S deficiency) (sinusoidal portal hypertension). HVPG is defined as the differ-
or acquired (such as myeloproliferative neoplasm) and/or local ence between WHVP and FHVP. It is based on the concept that
factors such as sepsis, abdominal trauma, pancreatitis or sur- when the blood flow in a hepatic vein is blocked by a ‘wedged’
gery are responsible for 70% of cases, whereas the remaining catheter, the static column of blood transmits the pressure from
30% are idiopathic. In children, portal vein thrombosis is often the preceding communicated vascular territory, in this case,
related to omphalitis or umbilical vein catheterization. Portal the hepatic sinusoids. Thus, WHVP is a measurement of the
vein thrombosis may present as two distinct clinical scenarios; hepatic sinusoidal pressure and not of portal pressure itself. As
acute or chronic (portal cavernoma); its diagnosis is based on in cirrhosis the intersinusoidal communications are lost due to
imaging techniques [7] . fibrosis, septa and nodule formation, the sinusoidal pressure
Intrahepatic portal hypertension can be further classified equilibrates with portal pressure. It is well demonstrated that
considering the site of increased resistance and the results of WHVP adequately reflects portal pressure in alcoholic liver
hepatic vein catheterization (see below). Presinusoidal portal disease [8] , hepatitis C- [8] and hepatitis B-related cirrhosis [9] ,
hypertension is characterized by normal or slightly increased which are the most frequent etiologies of chronic liver disease.
HVPG values, with normal or slightly increased wedged hepatic The use of balloon-tipped catheters is recommended to meas-
venous pressure (WHVP) and normal free hepatic venous pres- ure HVPG [1] , since the volume of the liver circulation that
sure (FHVP). Idiopathic portal hypertension, nodular regen- is ‘sensed’ is much larger than that obtained by wedging the
erative hyperplasia, schistosomiasis, sarcoidosis, tuberculosis catheter, which enhances the reliability and accuracy of the
and early stages of primary biliary cirrhosis are the main causes measurement [10] .
of presinusoidal intrahepatic portal hypertension. Sinusoidal
portal hypertension is found in most chronic liver diseases Technical aspects
(including secondary biliary cirrhosis) and is characterized by HVPG measurement is carried out at the hepatic hemo
an increase in WHVP with normal FHVP, resulting in high dynamics laboratory under light conscious sedation (midazolam
HVPG; cirrhosis is the most common cause. In postsinusoidal 0.02 mg/kg intravenously) [11] and with noninvasive vital sign
portal hypertension, HVPG is normal and both WHVP and monitoring (by electrocardiography, arterial blood pressure and
FHVP are increased, such as in the Budd–Chiari syndrome. In pulse oxymetry); under local anesthesia, with ultrasound assis-
some diseases hepatic vein catheterization can show the evolu- tance [12] , the right jugular vein (or the femoral or antecubital
tion of the pathology. For example, schistosomiasis in the initial vein) is catheterized, a venous introducer is placed and a balloon-
phase induces the formation of portal granulomas and fibrosis tipped catheter is guided under fluoroscopic control through the
obliterating portal venules (presinusoidal portal hypertension); right atrium and IVC into the main right hepatic vein.
HVPG is normal in this phase. Later on, fibrosis may extend FHVP is measured by maintaining the tip of the catheter ‘free’
out of the portal tract and cause sinusoidal portal hyperten- in the hepatic vein, at 2–4 cm from its opening into the IVC
sion, with high HVPG and a hemodynamic and clinical pattern (Figure 2A) . If the difference between FHVP and IVC pressure
resembling cirrhosis. is greater than 2 mmHg, it is likely that the catheter was inad-
Budd–Chiari syndrome is the most frequent cause of post equately placed, and the report should contain this information.
hepatic portal hypertension. The obstruction of hepatic venous It should be noted that right atrial pressure cannot substitute
outflow can be present from the small hepatic venules (and be FHVP for the measurement of HVPG [13] .
truly intrahepatic) up to the entrance of the IVC into the right The WHVP is measured by occluding the hepatic vein by
atrium. Budd–Chiari syndrome is usually caused by underlying inflating the balloon at the tip of the catheter (Figure 2B) . Adequate
prothrombotic disorders (mainly myeloproliferative disorders) occlusion of the hepatic vein is confirmed by slowly injecting
and its diagnosis is usually made by imaging techniques. 5 ml of contrast dye into the vein with the balloon inflated. This
procedure should reveal a typical wedged pattern, without reflux
Gold-standard technique to assess portal of the contrast dye or washout through communications with
hypertension: measurement of HVPG other hepatic veins. The existence of veno–venous communica-
The pressure gradient between the portal vein and the IVC (PPG) tions (Figure 2C) is very rare in cirrhosis, while it is commonly
represents the liver portal perfusion pressure; its normal value is observed in idiopathic portal hypertension [14,15] and in other
up to 5 mmHg. Direct measurements of portal pressure can be noncirrhotic portal hypertensive diseases. Therefore their pres-
performed through transhepatic or transvenous catheterization ence should be documented and reported. The WHVP should
of the portal vein. This technique further requires catheterizing be measured until the value remains stable (usually more than
the IVC to determine the PPG. Because of this and of the risk 60 s). All measurements should be taken in triplicate and perma-
of intraperitoneal bleeding, direct measurements of portal pres- nent tracings (Figure 2D) should be obtained using a multichannel
sure are rarely used and are limited to selected cases of presinu- recorder and adequately calibrated transducers.
soidal portal hypertension, such as in the case of patients with Some practical tips to achieve adequate measurements accord-
esophageal varices, patent portal vein and normal WHVP. ing to published recommendations [1,16] are outlined in Box 1.

There are no absolute contraindications to

HVPG measurement; the limitations of
the technique and the procedures that can
be performed during hepatic vein cathe-
terization (beside HVPG) are summarized
in Table 1.
Hepatic vein catheterization u sually
carries only a modest discomfort. Com
plications are infrequent (<1% of cases);
most of them are related to local injury at
the venous access site. This risk is markedly
reduced with the use of ultrasound guid-
ance for performing the venous puncture.
Passage of the catheter through the right
atrium rarely causes arrhythmias, which
are usually transient. In the authors’ expe-
rience no fatalities have occurred in over
12,000 procedures in 30 years.
Applications
Measurement of HVPG is a useful clini-
cal tool in hepatology and is currently Figure 2. Measurement of hepatic venous pressure. (A) FHVP is measured by
considered the best surrogate of clinical maintaining the tip of the catheter ‘free’ in the hepatic vein at 2–4 cm from its opening
events in liver diseases [17] . Its main clinical into the inferior vena cava. (B) WHVP is measured by occluding the hepatic vein by
applications are listed below. inflating the angiographic balloon (arrow) at the tip of the catheter. Adequate occlusion
of the hepatic vein is confirmed by slowly injecting 5 ml of contrast dye into the vein with
the balloon inflated. Please note the typical ‘wedged’ pattern distal to the balloon.
HVPG in the classification of portal (C) A washout of contrast dye through communications with other hepatic veins (arrow)
hypertension prevents a correct measurement of the hepatic venous pressure. (D) Typical tracing of
In patients with portal hypertension of pressures measured in the hepatic vein obtained using a multichannel recorder and
unknown causes the finding of an increased adequately calibrated transducers.
HVPG owing to an increase in WHVP FHVP: Free hepatic venous pressure; WHVP: Wedged hepatic venous pressure.
indicates an increase in sinusoidal pres-
sure, which is most frequently due to cirrhosis. A normal HVPG hypertension, while posthepatic portal hypertension features
with normal WHVP and FHVP is typical of presinusoidal portal increased FHVP and WHVP (Figure 1) .
Box 1. An abecedary of tips for obtaining adequate measurements of the HVPG.

• Amplitude of the scale in the recording system: use an appropriate scale for venous pressure measurements (full range 40 mmHg). Set
recorders at 1 mmHg = 1 mm paper. Amplitudes used for arterial pressure measurements are not adequate.
• Balloon catheter: use balloon-tipped catheters. These allow occlusion of a medium size or large hepatic vein, minimize variability and
facilitate repeat measurements. Check for adequate occlusion of the hepatic vein and for absence of communications between hepatic
veins by injecting by hand 5 ml of iodinated contrast.
• Calibrate: the transducer should be calibrated against known external pressures before starting measurements (e.g., 13.6 cm H2O
should read 10 mmHg, 27.2 cm H2O should read 20 mmHg and 40.8 cm H2O should read 30 mmHg). Transducers that do not calibrate
exactly should be discarded. Place the transducer at the level of the right atrium (mid-axillary line). With transducer open to air
(zero pressure) adjust the recorder to read zero.
• Duplicate measurements: do all measurements at least by duplicate (by triplicate if differences between measurements are >1 mmHg).
Variability often reflects mistakes.
• Events: any event that may cause an artifact, such as coughing, moving or talking should be noted.
• Free pressure: FHVP should be measured with the catheter tip less than 4 cm in the hepatic vein. FHVP should not exceed IVC pressure
by more than 2 mmHg. IVC pressure should be measured at the level of the hepatic vein ostium.
• Get permanent tracings: all measurements should be recorded on a permanent data recording system (paper printouts and/or digital
memory), to allow subsequent review of the pressure tracings. Readings from a monitor screen are not adequate.
• Hold-on: venous pressures should be allowed to stabilize over a period of at least 1 min for WHVP and 20 s for FHVP (some patients may
require longer). A slow speed (<5 mm/s) should be used in the recorder. Rinse the catheter with 5% dextrose before any measurement.
FHVP: Free hepatic venous pressure; IVC: Inferior vena cava; WHVP: Wedged hepatic venous pressure.
Table 1. Hepatic venous pressure gradient measurement: relative contraindications, limitations and
associated procedures.
Relative contraindications Limitations Associated procedures
Allergy to iodine contrast medium: iodine HVPG does not reflect the PPG when increased resistance is Transjugular liver biopsy
contrast can be avoided and CO2 can be predominantly located at presinusoidal sites (portal vein
used instead thrombosis; schistosomiasis, initial stages of primary biliary
cirrhosis; idiopathic portal hypertension)
Previous episodes of cardiac arrhythmia: Check for the absence of communications between hepatic Measurement of hepatic
caution when moving the catheter in the veins that may preclude an adequate measurement of WHVP blood flow and liver
right cardiac atrium clearance by ICG infusion
Platelet <20,000 or PT <30%: platelet and Wedged hepatic retrograde
frozen plasma replacement can be used if portography using CO2 as
needed contrast medium
HVPG: Hepatic venous pressure gradient; ICG: Indocyanine green; PPG: Portal pressure gradient; PT: Prothrombin time; WHVP: Wedged hepatic venous pressure.
Prognostic stratification in patients with cirrhosis & acute within 48 h of admission) predicts failure to control bleeding
alcoholic hepatitis and low 1-year survival [22] . In patients with decompensated
The HVPG is a strong independent prognostic indicator in cirrhosis listed for liver transplantation HVPG holds prognostic
compensated and decompensated cirrhosis. Table 2 summarizes value independent from that of model for end-stage liver disease
prognostic value of different HVPG thresholds in patients with (MELD) score [23] . Liver resection for hepatocellular carcinoma
cirrhosis (not undergoing therapy with β-blockers). is contraindicated in patients with HVPG >10 mmHg [24,25]
Cross-sectional and prospective clinical hemodynamic stud- due to a high risk of irreversible hepatic decompensation within
ies have shown that in compensated patients the complications 3 months.
of portal hypertension, such as ascites, variceal formation and Portal pressure may increase during episodes of acute alco-
hepatorenal syndrome do not occur until the HVPG is at least holic hepatitis and HVPG >22 mmHg is associated with a poor
10 mmHg [3,18] . Therefore, portal hypertension is ‘subclinical’ survival. This emphasizes the relevance of measuring HVPG at
when the HVPG is 6–9 mmHg and becomes ‘clinically signifi- the time of transjugular liver biopsy in these patients. Steatosis
cant’ when HVPG increases above 10 mmHg. While patients may also concur to increase the HVPG in nonalcoholic fatty
with a HVPG below 10 mmHg are at negligible risk of experi- liver d isease but the prognostic significance of this finding is
encing portal hypertension-related complications, patients with unknown [21] .
a HVPG over 10 mmHg are at an increased risk of decompensa-
tion and of hepatocellular carcinoma [19] . Variceal bleeding may Assessment of the hemodynamic response to pharmacological
appear when HVPG is over 12 mmHg. An increased mortal- therapy for portal hypertension
ity risk is observed when HVPG is above 16 mmHg [20,21] and A good hemodynamic response is defined as a reduction of HVPG
during acute variceal bleeding a HVPG >20 mmHg (measured below 12 mmHg or at least by 20% of the baseline value, either
by means of pharmacological treatment
Table 2. Prognostic significance of hepatic venous pressure gradient or due to an improvement in liver dis-
thresholds according to the compensated or decompensated stage of ease [26] . When this target reduction is
cirrhosis. accomplished, the risk of variceal bleed-
ing, rebleeding and other complications of
Clinical HVPG Increased risk of threshold portal hypertension such as ascites, spon-
setting (mmHg)
taneous bacterial peritonitis and hepato-
Compensated 10 Presence [18] and development of gastroesophageal varices [2] renal syndrome markedly decreases and
cirrhosis First clinical decompensation in patients without varices [76] survival improves [26] . Failure to achieve
Development of HCC [19]
these targets (reduction below 12 mmHg
Decompensation after surgery for HCC [24,25]
12 Variceal bleeding [18,20,77–79] or more than 20% from baseline) consti-
16 First clinical decompensation in patients with varices [80] ; tutes the strongest independent predictor of
mortality [81] variceal bleeding or rebleeding [26] . Given
Decompensated 16 Variceal rebleeding and mortality [21] these observations, it has been suggested
cirrhosis 20 Failure to control variceal bleeding in patients actively that the treatment of portal hypertension
bleeding from varices [22,50] ; mortality should be individualized by measuring the
22 Mortality in patients with alcoholic cirrhosis and AAH [82] portal pressure response to therapy in order
30 Spontaneous bacterial peritonitis [83] to maximize clinical effectiveness. The
AAH: Acute alcoholic hepatitis; HCC: Hepatocellular carcinoma; HVPG: Hepatic venous pressure gradient. need of repeated measurements of HVPG

may be reduced by testing the acute hemodynamic response to include both medium and large varices, grading can be simplified
intravenous β-blockers [27,28] . to ‘small’ (≤5 mm) and ‘large’ varices [33] . The presence of ‘red
wales’ (longitudinal dilated venules resembling whip marks on the
Evaluation of progression & regression of chronic liver disease variceal surface) or ‘red spots’ should be assessed and reported, as
Chronic viral hepatitis they are associated to increased bleeding risk and prompt primary
HVPG has been shown to correlate with the histological severity prophylaxis even in patients with small varices [34] . A similar
of liver fibrosis in patients with HBV- and HCV-related chronic increase in bleeding risk occurs with more advanced liver failure
hepatitis [8] . Moreover, HVPG changes parallels changes in his- (Child–Pugh classes B–C).
tology after effective antiviral therapy. Rincon et al. [29] showed Gastric varices are less prevalent than EV and are the source
a significant HVPG reduction after effective antiviral therapy 5–10% of upper digestive bleeding episodes in cirrhosis. They are
in patients with advanced chronic HCV hepatitis. This was commonly classified based on their relationship with esophageal
confirmed in patients with HCV-related cirrhosis achieving sus- varices as well as their location [35] . Gastroesophageal varices are
tained virological response [30] . Thus, serial HVPG measurements an extension of esophageal varices and are subclassified into two
allow evaluating progression/regression in chronic hepatitis C and types: GOV1, the most common, extend along the lesser curva-
evaluating the response to antiviral treatment [31] . ture. GOV2 extend from EV along the fundus. Isolated gastric
varices (IGV) in absence of EV may be located in the fundus
HCV recurrence after liver transplantation (IGV1; splenic vein thrombosis must be ruled out), while IGV2
HVPG is an excellent marker to identify patients at highest risk are located in the body, antrum or along the pylorus. As for EV,
of severe HCV recurrence and hepatic decompensation after liver the presence of red spots, gastric variceal size and Child–Pugh
transplantation. Portal hypertension, as indicated by HVPG class (C>B>A) are risk factors for hemorrhage. GOV1 and IGV
>6 mmHg, accurately selected patients at risk of cirrhosis recur- may bleed at relatively low HVPG (10–12 mmHg); this might
rence and worsening of liver function [1] , in fact this was bet- be due to the fact that these varices are usually very large and
ter than liver biopsy. HVPG changes mirrored the changes in therefore their wall tension (which is determined as the product
liver histology induced by antiviral therapy in liver transplant of transmural pressure and vessel radius) may reach high values
recipients with recurrent HCV infection [32] . at a lower pressure than EV.
PHG is a very common finding in cirrhosis (prevalence between
Evaluation of PPG after TIPS placement 11 and 80%). It is graded as mild (mosaic-like pattern), and severe
The measurement of PPGt (the gradient between portal pressure (red-point lesions/cherry-red spots/black-brown spots) [33] , and is
and IVC pressure) during and after transjugular intrahepatic more often observed in the fundus and corpus of the stomach.
porto–systemic shunt (TIPS) placement is the gold-standard Gastric antral vascular ectasia (GAVE), also known as water-
technique to assess its correct hemodynamic functioning. The melon stomach, is endoscopically characterized by red patches
TIPS target is to decrease the PPG below 12 mmHg [3] . In the and spots in a diffuse or linear distribution in the gastric antrum.
follow-up TIPS is considered to work properly if PPG remains Other typical features include gastric ectasia and dilation and
below 12 mmHg. Above this threshold TIPS dysfunction is biopsy can identify thrombi, spindle cell proliferation and
diagnosed, which should be corrected by balloon angioplasty ﬁbrohyalinosis. Only 30% of GAVE cases occur in patients with
or restenting to prevent recurrence of complications of portal portal hypertension and GAVE should not be considered a portal
hypertension [3] . hypertension-specific feature. In particular, GAVE should be dis-
tinguished from severe PHG [36] owing to their different response
Gold-standard technique to assess the presence of to the treatment of portal hypertension. While β-blockers and
gastroesophageal varices: endoscopy TIPS can be used in severe PHG causing significant blood losses,
Upper GI tract endoscopy is the gold-standard technique for GAVE is unresponsive to these treatments [37] .
identifying esophageal and gastric varices and is essential for the
endoscopic management of variceal hemorrhage [33] . Deep seda- Use of endoscopy in clinical practice: screening &
tion with propofol (±fentanil or remifentanil) much improves the follow-up of EV
acceptability of endoscopy and patients’ comfort. EV is present in approximately 30–40% of compensated cir-
Diagnostic endoscopy findings related to portal hypertension rhosis at first observation and up to 60% of decompensated cir-
are esophageal varices (EV), gastric varices and PHG. Rarely, rhosis. There is consensus that it is mandatory to screen for EV
ectopic duodenal varices can be found. The risk of bleeding from by endoscopy when the diagnosis of cirrhosis is established. In
EV is tightly related to their size and presence of so-called ‘high- patients without varices, incidence of EV is 5–10%/year; endos-
risk signs’ [34] . Size of EV is semiquantitatively graded as small, copy must therefore be repeated every 2–3 years in this population
medium or large [34] . Small varices are minimally elevated veins [33] . Patients with an HVPG >10 mmHg or with liver function
that collapse but do not disappear with insufflation, medium deterioration are at higher risk for developing varices, so the inter-
varices are tortuous veins occupying less than a third of the val could be shortened. In patients with small varices, increase in
esophageal lumen and large varices are those involving more size is observed with a 10–15% annual incidence; hence, in this
than a third of the lumen. Since treatment recommendations population endoscopy should be repeated every 1–2 years [33] . In
patients undergoing primary pharmacological prophylaxis there posthepatic portal hypertension: in patients with portal vein
is no need of performing follow-up endoscopies [33] . thrombosis liver biopsy should be performed only when concomi-
tant cirrhosis or nodular regenerative hyperplasia is suspected.
Other endoscopic techniques used in the field of portal In Budd–Chiari syndrome, liver biopsy should be considered
hypertension when imaging fails demonstrating large hepatic veins or IVC
Endoscopic videocapsule obstruction but the odds for a Budd–Chiari syndrome diagno-
This has been recently introduced as it may improve patients’ sis remains high [7] . Liver biopsy is the gold standard for the
tolerance and adherence for the screening and surveillance of EV. diagnosis of cirrhosis. Limitations of the technique include false-
First studies and a meta-analysis reported a correct identification negative results or underestimation of the disease severity due
of EV and red wale marks in about 80% of cases, but subsequent to a sampling error and inter- and intra-observer variability, in
studies disclosed a lower diagnostic value [38] . Videocapsule weak- particular in macronodular cirrhosis. Liver biopsy can provide
nesses are a poor diagnostic value for gastric varices and PHG, a information on the severity of portal hypertension in patients with
poor cost–effectiveness ratio, difficulties in assessing variceal size cirrhosis: small nodule size and increased septal thickness were
and nonapplicability in 6% of patients who can not swallow the associated with higher HVPG [45] and clinical decompensation.
pill-cam. Portal enteropathy has been recently characterized by Recently, quantitative computer-assisted digital-image analysis
videocapsule and enteroscopy, describing several types of mucosal (DIA) of histological liver sections has been validated for assess-
abnormalities such as edema, erythema, reticular mucosal pat- ing liver fibrosis (as fibrosis area). Limitations of DIA include
tern and small bowel varices. Videocapsule is a useful tool in the use of additional resources, and require evaluating inter- and
diagnosing obscure sources of bleeding (small bowel varices and intra-observer variability. Studies showed that DIA is a better
vascular ectasias) [39] . histological index that traditional stage scores (e.g., Ishak score)
and should be used in future studies validating liver stiffness (LS)
Endoscopic ultrasound and other noninvasive markers of fibrosis. Calvaruso et al. showed
Endoscopic ultrasound provided with color- or power-Doppler that the degree of fibrosis of liver biopsies, measured using DIA,
can be useful in diagnosing IGV that may mimic thickened gas- correlated well with HVPG in 115 patients with post-transplant
tric folds and it has shown to improve the efficacy of cyanocrilate HCV infection, including all stages of fibrosis [46] . These results
injection for the treatment of gastric varices [40] . were further validated by another study showing that the fibrosis
area measured by DIA correlated with HVPG in patients with
Measurement of variceal pressure cirrhosis [47] .
Variceal pressure can be measured at endoscopy either by direct
variceal puncture (which is hampered by the risk of precipitat- Noninvasive techniques to assess portal hypertension
ing variceal bleeding) or using a noninvasive endoscopic pres- HVPG and endoscopy are current gold-standard techniques to
sure sensitive gauge [41] . The latter technique has been shown to assess portal hypertension and esophageal varices. However its use
be accurate for assessing variceal pressure and its changes after is limited by their invasiveness. Patients would undoubtedly ben-
either acute or chronic pharmacological therapy [42] and provides efit from noninvasive tests that are able to provide similar infor-
prognostic information. However, measurements are difficult in mation. As any diagnostic test, noninvasive techniques should
small varices and require specific training. Currently, its use is be safe, easy to perform, inexpensive, accurate and reproduc-
limited to research studies. ible. Ideally, such tests should be predictive of long-term c linical
outcomes.
Liver biopsy as a technique to improve knowledge
concerning portal hypertension Clinical data & physical examination
Liver biopsy has been used for several indications: diagnosing and In the absence of anamnestic data, the cheapest and most immedi-
grading liver diseases, and to guide therapeutic d
ecisions [43] . It can ate information on presence of portal hypertension is that p rovided
be performed either by percutaneous or transvenous (transjugular) by physical examination; splenomegaly, spider nevi, presence of
routes. The latter is performed during hepatic vein catheterization, abdominal wall collateral circulation and ascites (±edema) are
is safer and preferable in high-risk patients (due to thrombope- highly specific of the syndrome [48] , but the sensitivity of physical
nia or ascites) and has the advantage of adding histological and signs is low in patients with compensated cirrhosis. In a recent
hemodynamic information in the same procedure. study in patients with well-compensated cirrhosis, spider nevi
An adequate liver specimen should be of at least 15 mm length were independent predictors of esophageal varices [49] .
and contain ≥6 complete portal tracts; ideally, specimens should
be 20–25 mm and have ≥11 portal tracts [44] . Limitations of liver Laboratory tests
biopsy include its invasiveness and sampling errors due to under- A further step is represented by laboratory tests, having the advan-
representation of liver pathology as biopsy specimens account for tage of being inexpensive and independent of expertise. Albumin,
only 1 out of 50,000 of the liver parenchyma. bilirubin, international normalized ratio (INR) or their combi-
Liver biopsy has a key role in the differential of intrahepatic nation in the Child–Pugh score correlate with HVPG [21,50] and
causes of portal hypertension, but is marginal in prehepatic or with the prevalence and grade of esophageal varices in cirrhotic

Table 3. Prediction of clinically significant portal hypertension by transient elastography.

Study (year) Patients Etiology Design Patients Correlation Prediction of CSPH Ref.
(n) with CSPH of LS and (HVPG ≥10 mmHg)
(%) HVPG (R) Cutoff AUC
Vizzutti et al. (2007) 61 HCV Prospective 77 0.81 13.6 0.99 [60]
Lemoine et al. (2008) 48 Alcohol Retrospective 83 0.76 34.9 0.94 [84]

HCV 77 20.5 0.76
Bureau et al. (2008) 150 Several Prospective 51 0.86 21.0 0.94 [85]
Sanchez-Condé et al. 38 HIV-HCV Prospective 74 0.68 14.0 0.80 [86]

(2011)
Llop et al. (2012) 79 Several + potentially Prospective 41 0.55 20.6 0.84 [59]
resectable HCC
AUC: Area under the curve; CSPH: Clinically significant portal hypertension; HCC: Hepatocellular carcinoma; HCV: Hepatitis C virus; HVPG: Hepatic venous pressure
gradient; LS: Liver stiffness.
patients. In a study from our group in patients with compen- 0.77–0.99) of TE for diagnosing and ruling-out CSPH (HVPG
sated cirrhosis, a model combining albumin, ALT and INR had >10 mmHg) in patients with cirrhosis (Table 3) [57] , LS showing a
an area under the curve (AUC) of 0.952 in predicting clinically significant linear correlation with HVPG (R range: 0.55–0.86).
significant portal hypertension (CSPH; HVPG >10 mmHg) [49] . The cutoff for predicting CSPH varies across studies, mainly due
Thrombocytopenia is the single laboratory test most frequently to differences in the choice of sensitivity or specificity. This limita-
associated with the presence of varices and of large esophageal tion is largely overcome by applying a pragmatic rule, choosing a
varices [51] . very sensitive cutoff to rule-out CSPH and a very specific cutoff
Most serum fibrosis markers have not been specifically studied to rule it in. In doing so, a LS <13.6 kPa confidently rules-out
in predicting portal hypertension but some data suggest that they CSPH, while LS ≥21.1 kPa accurately diagnoses it. Interestingly,
might be useful. Fibrotest showed a good accuracy in one study a recent study [58] showed that both HVPG ≥10 mmHg and LS
[52] , but as 92% of the studied population had CSPH its speci- ≥21.1 kPa were good predictors of clinical decompensation, with
ficity is questionable. YKL-40 and collagen propeptide PIIINP substantially equal discriminative ability (AUC: 0.815 vs 0.837;
were predictive of short-term survival and increased relative-risk not significant). On the other hand, patients with intermediate
of death in patients with alcoholic liver disease [53] ; hyaluronic values (LS between 13.6 and 21.1 kPa) cannot be easily classified
acid had a predictive value equivalent to Child–Pugh score in a as having or not having CSPH. This was also shown recently
cohort of patients with HCV-related cirrhosis followed-up for a in patients with potentially resectable hepatocellular carcinoma,
median of 38 months [54] . indicating that TE might be used to rule-out or confirm CSPH,
and thus for indicating or contraindicating surgery [59] whenever
Measurement of LS by transient elastography HVPG is not available.
Transient elastography (TE; Fibroscan®, Echosens, Paris, France) On the other hand, it should be underlined that above the
is a well-validated technique for the noninvasive assessment of threshold value of 13.6 kPa the correlation of LS and HVPG is
liver fibrosis [55] . Measurements are performed with an ultra- less accurate [60] , probably reflecting that at HVPG >10 mmHg
sound transducer built on the axis of a vibrator; a vibration of development of portals–systemic collaterals and increased por-
mild amplitude and low frequency is transmitted, inducing a tal–collateral blood flow means that fibrosis is no longer the main
wave that propagates through the liver tissue, and pulse-echo mechanism responsible for portal hypertension [60] . This also
acquisitions are performed to measure the velocity of propaga- partially explains why TE is not accurate enough to predict the
tion of the wave, which is directly related to tissue stiffness. presence and size of esophageal varices (accuracy does not exceed
Since fibrosis is the main determinant of tissue stiffness and of 65–75% in the published studies with adequate sample size). In
hepatic resistance to portal blood flow (the major determinant summary, TE can be very useful to rule out or rule in CSPH, but
of portal pressure in early stages of portal hypertension), TE has there is a considerable ‘gray zone’ (between 13.6 and 21.1 kPa)
been tested in recent years as a novel way of obtaining numerical, and the technique is not accurate enough to substitute HVPG to
objective and operator-independent noninvasive surrogate data quantify the exact severity of portal hypertension. Major tech-
of HVPG [55] . nical limitations of TE include the lack of visualization of the
In a study performed in patients with hepatitis C recurrence parenchyma in the region of interest and failure to obtain any
after liver transplantation, LS showed a good linear correlation measurement or unreliable results in 3–16% of cases [61] mostly
with fibrosis and HVPG [56] ; specifically, a LS ≥8.74 kPa had a because of obesity or presence of ascites. Moreover, the influence
sensitivity and specificity of 90 and 81%, respectively, for the of the etiology of cirrhosis (e.g., alcoholic vs viral cirrhosis) on the
diagnosis of HVPG >6 mmHg in this population. Five subse- cutoffs of TE for CSPH have not been specifically studied, and
quent studies provided evidence of a good accuracy (AUC range: should be addressed by future studies.
Newer methods for estimating LS include magnetic reso- (patent paraumbilical vein, spleno–renal collaterals, dilated left-
nance imaging elastography (MRE) [62] and ultrasound-based and short-gastric veins), and inversion of flow within the portal
(sonoelastography) methods (strain ratios, acoustic radiation system are 100% specific of CSPH. Some collaterals, such as left-
force impulse imaging [ARFI] and shear-wave velocity estima- gastric vein >3 mm and short-gastric veins, strongly suggest the
tion). While MRE is accurate but too costly to be routinely presence of esophageal varices, and their development/increase in
used, sonoelastography is increasingly used, as it can be imple- number have been associated with a greater proportion of variceal
mented on ultrasound equipment and overcome technical formation and growth [67,69] .
limitations of TE. Among sonoelastography methods ARFI On the other hand, it should be underlined that US and
(Virtual Touch™ Tissue Quantification; Siemens Healthcare, Doppler-US are very accurate for detecting portal vein and hepatic
Erlangen, Germany) is the best validated so far. ARFI uses veins thrombosis [70] . As portal vein thrombosis often takes place
mechanical excitation of the tissue using short-duration (262 µ) in patients with cirrhosis and hepatocellular carcinoma, which
that propagate shear waves and generate localized, µ-scale dis- can be detected by US, and can aggravate a previously stable
placements in tissue. The shear-wave velocity (expressed in m/s) condition, US should be routinely performed to rule-out these
is measured in a 10-mm long and 6-mm wide region that can complications in patients with cirrhosis presenting a new clinical
be chosen by the operator on real-time imaging. ARFI has event [67] .
already shown to hold a similar accuracy as TE in predicting Splenomegaly is the most common and sensitive sign of portal
significant fibrosis and cirrhosis [63] and preliminary data in hypertension. It is an independent predictor of esophageal varices,
assessing the consequences of portal hypertension suggest simi- and is a marker of CSPH in compensated cirrhotic patients.
lar results. An important limitation that is probably inherent to Progressive spleen enlargement has been shown to predict variceal
all elastography techniques is that LS can increase independent formation and growth, and is associated with a higher probability
of fibrosis due to food ingestion, inflammation, cholestasis and of clinical decompensation [67,69] .
liver congestion. Other US and Doppler-US signs of CSPH include dilatation of
portal vein (diameter >13 mm); lack or reduced respiratory vari-
Spleen stiffness ations of splenic and superior mesenteric vein diameter; reduced
Since splenomegaly in cirrhosis is a direct consequence of por- portal vein velocity; increased ‘congestion index’ of portal vein;
tal hypertension, spleen stiffness has been recently proposed as altered hepatic vein Doppler pattern; increased intraparenchy-
a new noninvasive parameter with better accuracy than LS for mal hepatic and splenic artery resistance and pulsatility index;
predicting CSPH and esophageal varices. Data obtained by MRE increased intraparenchymal renal artery resistance and pulsatility
[64] , TE [65] , real-time elastography [66] and ARFI appear promis- index and reduced mesenteric artery resistance and pulsatility
ing, and future studies assessing the performance of noninvasive index [67,69] . While US signs can reliably indicate CSPH, the cor-
predictors of portal hypertension should include this parameter. relation of HVPG with these parameters is unsatisfactory; thus
US signs can not be used as surrogates of HVPG.
Imaging techniques: ultrasound & US are highly sensitive in diagnosing ascites, which is the most
color Doppler ultrasound common clinical decompensation of cirrhosis and holds a severe
Ultrasonography (US) is the first-line imaging technique recom- prognostic significance. Also, increased intrarenal arteriolar resist-
mended for the diagnosis and follow-up of patients with por- ance index correlates with renal vasoconstriction in patients with
tal hypertension [67] , since it is noninvasive, cheap and can be cirrhosis; it is observed in about 40% of patients with ascites and
performed at bedside. US is highly specific for the diagnosis of is accurate in detecting hepatorenal syndrome. Small liver size,
cirrhosis and portal hypertension, but its sensitivity is relatively splenomegaly >14.5 cm, mean portal vein velocity below 10 cm/s
low in compensated patients. Diagnosis of cirrhosis on conven- and loss of pulsatility of hepatic veins have been all associated
tional US is based on changes in liver morphology and signs with higher mortality on follow-up in patients with compensated
of portal hypertension [67] . The most accurate single US sign cirrhosis [67,69] .
for the diagnosis of cirrhosis is nodularity of liver surface. This US-Doppler is useful in the noninvasive follow-up of TIPS [71] .
should be specifically investigated using high-frequency trans- However, US-Doppler is insufficiently accurate to be used as a
ducers, with better diagnostic performance than conventional surrogate of changes of HVPG during medical therapy of portal
abdominal US probes. The combination of nodular liver surface hypertension [67,69] .
and portal flow mean velocity <12 cm/s has 80% accuracy dis-
criminating patients with chronic hepatitis with severe fibrosis CT scan & MRI
from those with cirrhosis and its combination with TE allows CT and MRI allow a very accurate visualization of the portal
an optimal accuracy in ‘difficult’ patients [68] . In patients with venous system. Single detector and multidetector CT scanning
known cirrhosis, US-Doppler has >80% specificity diagnosing are reliable in detecting large esophageal varices (specificity:
CSPH, but sensitivity does not exceed 40–70%, particularly in 90–100%; sensitivity: 84–100%), with moderate interobserver
compensated patients [67] . While the presence of one or more variability; however, the sensitivity in detecting small varices is
signs allows establishment of a robust diagnosis, their absence lower. CT screening of varices was more cost-effective than endos-
cannot exclude CSPH. The presence of portal–systemic collaterals copy screening and than CT followed by endoscopy in patients

with small varices on CT. However, CT scan implies substantial characterization of esophageal and gastric varices) we currently
irradiation, which should be carefully considered in risk–ben- have to rely on invasive techniques (even if these are moderately
efit assessment. Dynamic contrast-enhanced single-section CT invasive), such as hepatic vein catheterization for the measure-
scans and compartmental analysis of time/intensity curves of liver ment of HVPG, endoscopy to evaluate the presence, size and
MRIs after injection of a gadolinium chelate allow a quantitative aspect of the varices, and liver biopsy to confirm cirrhosis and
measurement of portal and azygos blood flow [72] . Portal fraction to perform an histological diagnosis in doubtful cases. These
of liver perfusion and mean transit time on MRI show a moderate methods have the advantage of being very robust and well vali-
correlation with HVPG [73] . dated and do not require complicated technology (thus being
CT and/or MRI should be used in clinical situations requir- available in most settings of healthcare delivery). However,
ing a detailed assessment of the portal venous system, such as to invasiveness imposes limitations in terms of cost and patients’
assess the extent of thrombosis; to detect portal cholangiopathy discomfort, thus restricting the use of these techniques. Clearly,
in patients with a portal cavernoma; to map collateral circula- if these were truly noninvasive their use would be much more
tion in patients with ectopic variceal bleeding, and before TIPS extensive.
placement, especially in ‘difficult’ patients, such as those with Is that going to change in years to come? As commented
Budd–Chiari syndrome. upon in this review, we are already there for some aspects as
the detection of CSPH (equivalent to an HVPG ≥10 mmHg),
Combination of different noninvasive methods since techniques as TE [55] , precise measurements of spleen size
The combination of different methods provides theoretical advan- by ultrasound, liver surface nodularity analysis and combined
tages over the use of a single method, since falsely positive and/or indices/algorithms based on these already allow sufficient sen-
negative results of one method may be overcome by the use of sitivity and specificity (above 80–90%) to permit a fair clinical
another, and complementary information may lead to more robust judgment. Still, it remains to be proved if these noninvasive tools
predictions. allow equally accurate estimates in different etiologies of cirrhosis
There are scarce data on the prediction of CSPH (as assessed and in situations such as after removal of the cause of cirrhosis by
by HVPG) by a combination of tests. A study performed before successful etiological therapy.
TE showed that the combination of simple laboratory tests (INR, We are a little bit more distant from noninvasive diagnosis
albumin and ALT) allowed predicting CSPH in patients with with regards to detection of varices, as the techniques that can
compensated viral cirrhosis [49] , but external validation showed be used as an alternative for endoscopy are either too expensive
less accuracy than that observed in the original series. As for and of uncertain sensitivity (such as the pill-cam) or carry other
the prediction of varices, platelet count and spleen diameter are inconveniences (such as radiation exposure and risk from CT
almost invariably found among the combinations tested in cirrho- scans). In this field the authors’ personal bet regards the use of
sis. Platelet count to spleen diameter ratio improves the predictive new developments in 3D contrast ultrasound using new trans-
ability of the two tests as assessed separately and values >909 had ducer technology, which has a strong potential for substituting
100% negative-predictive value for the presence of esophageal CT/MR scans at a much lower cost and at the bedside. As for
varices in the original study [74] , suggesting that endoscopy could noninvasive measurements of HVPG, the authors do not foresee
be avoided in these patients. However, subsequent independent any clinically applicable substitute with enough accuracy at short
series showed a quite lower predictive value. Other models for time, this is an unfulfilled need that deserves more research given
predicting varices of any size or large varices included portal vein the many applications of this technique. This is particularly so
diameter and prothrombin time [38] . Again, while initial prospec- for the applications requiring an exact measurement, such as
tive studies in compensated cirrhosis suggested good discriminat- assessing the effects of therapy, for which noninvasive methods
ing ability, validation series failed to confirm adequate predictive are unlikely to be accurate enough. On the other hand, this
accuracy. situation is a typical case of where one would like to be able
A recent study in patients with compensated hepatitis B cir- to check periodically if the treatment applied is reaching the
rhosis suggested that the combination of LS, spleen size and plate- desired targets, similar to what is done in the treatment of arte-
let count in the so-called LSPS (LS × spleen size/platelet count) rial hypertension with sphygmomanometers, which are a proven
is very accurate in predicting the presence of varices, high-risk valid noninvasive method to measure arterial blood pressure in
varices and variceal bleeding [75] . This promising noninvasive clinical practice. Even considering that our armamentarium to
approach should be validated by further studies, including other decrease portal pressure has been expanding, it is difficult to
etiologies of cirrhosis, before its use can be recommended in conceive that a given drug, or drug combination, will provide
clinical practice. adequate coverage for most patients as to allow obviating to
check the degree of portal pressure reduction actually achieved
Expert commentary & five-year view by the treatment. Personalized medicine would undoubtedly
We have very good methods for the evaluation of portal benefit markedly from such a portal sphygmomanometer, espe-
hypertension in chronic liver diseases. Unfortunately, for the cially in high-risk situations, such as primary prophylaxis in
more relevant aspects (detection of portal hypertension, its decompensated patients with large varices or in the prevention
severity, degree, changes during therapy and detection and of rebleeding.
Key issues
• Hepatic venous pressure gradient (HVPG) measurement is the gold-standard technique for the assessment of portal hypertension in
cirrhosis.
• Endoscopy is the gold-standard technique for diagnosing gastroesophageal varices.
• The use of HVPG in portal hypertension ranges from diagnostic purposes to prognostic stratification and guidance of therapy. HVPG is
currently the best surrogate marker of clinical events in cirrhosis.
• Noninvasive evaluation is a rapidly evolving field. Currently used techniques include laboratory parameters, imaging and elastography.
• Noninvasive techniques cannot replace HVPG and diagnostic endoscopy.
• Transient elastography, alone or combined with other parameters, allows discrimination with good accuracy for patients with and
without clinically significant portal hypertension, thereby reducing the need for invasive diagnostic procedures.
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Assessing portal hypertension in liver diseases
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1. You are seeing a 55-year-old man with a history of chronic hepatitis C virus infection as well as heavy alcohol use.
He has not had regular follow-up with a physician, and you are concerned regarding his risk for portal hypertension
and cirrhosis. What should you consider regarding the initial evaluation for this patient?
£ A The sensitivity of physical signs for portal hypertension is superior to their specificity
£ B A reduced serum albumin level is the most accurate laboratory assessment to identify varices
£ C Ultrasound is highly specific for the diagnosis of cirrhosis and portal hypertension
£ D The most accurate ultrasound sign of cirrhosis is reduced liver size
2. The patient’s initial evaluation suggests that he has cirrhosis. What should you consider regarding the assessment
of gastroesophageal varices in this case?
£ A Varices are considered large only if they occlude more than half of the esophageal lumen
£ B Gastric varices result in as many cases of gastrointestinal bleeding as esophageal varices
£ C Gastric antral vascular ectasia (GAVE) is only present in cases of portal hypertension
£ D Surveillance endoscopy should be repeated every 2 to 3 years among patients with cirrhosis
3. The patient eventually undergoes measurement of hepatic venous pressure gradient (HVPG) with a venous
catheter. Given his history of cirrhosis due to chronic hepatitis C virus infection and excessive alcohol use, what are
the expected findings on this testing?
£ A Normal HVPG and slightly increased wedged hepatic venous pressure (WHVP)
£ B Slightly increased HVPG and reduced WHVP
£ C Normal HVPG, elevated free hepatic venous pressure (FHVP), and elevated WHVP
£ D Normal FHVP, elevated HVPG, and elevated WHVP
4. Which of the following values for HVPG is considered the threshold for clinically significant portal hypertension?
£ A 10 mm Hg
£ B 16 mm Hg
£ C 20 mm Hg
£ D 33 mm Hg

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Expert Review of Gastroenterology & Hepatology

ISSN: 1747-4124 (Print) 1747-4132 (Online) Journal homepage: https://www.tandfonline.com/loi/ierh20

Assessing portal hypertension in liver diseases

Annalisa Berzigotti, Susana Seijo, Enric Reverter & Jaime Bosch

To link to this article: https://doi.org/10.1586/egh.12.83

Published online: 10 Jan 2014.

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Assessing portal hypertension

Release date: 28 January 2013; Expiration date: 28 January 2014

www.expert-reviews.com 10.1586/EGH.12.83 © 2013 Expert Reviews Ltd ISSN 1747-4124 141

Financial & competing interests disclosure

Definition Portal hypertension is an almost unavoidable consequence

Natural history Pathophysiology

142 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

144 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

There are no absolute contraindications to

Box 1. An abecedary of tips for obtaining adequate measurements of the HVPG.

146 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

148 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

Table 3. Prediction of clinically significant portal hypertension by transient elastography.

Lemoine et al. (2008) 48 Alcohol Retrospective 83 0.76 34.9 0.94 [84]

Sanchez-Condé et al. 38 HIV-HCV Prospective 74 0.68 14.0 0.80 [86]

150 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

152 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

154 Expert Rev. Gastroenterol. Hepatol. 7(2), (2013)

Assessing portal hypertension in liver diseases

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