combined liver vein and spleen pulp pressure measurements in patients with portal or splenic vein...
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Combined Liver Vein and Spleen Pulp Pressure Measurements in Patientswith Portal or Splenic Vein Thrombosis
S. Keiding, J. Solvig, H. Grønbæk & H. VilstrupDept. of Medicine V (Hepatology and Gastroenterology), PET Centre and the Dept. of Radiology,Aarhus University Hospital, Aarhus, Denmark
Keiding S, Solvig J, Grønbæk H, Vilstrup H. Combined liver vein and spleen pulp pressure measurementsin patients with portal or splenic vein thrombosis. Scand J Gastroenterol 2004;39:594–599.
Background: Patients with thrombosis of the portal or splenic vein may develop portal hypertension withbleeding from oesophageal or gastric varices. The relevant portal pressure cannot be measured by livervein catheterization or transhepatic puncture of the portal vein because the obstruction is peripheral to theaccessible part of the portal system.Methods: Liver vein catheterization was combined with percu-taneous splenic pressure measurement in 10 patients with portal or splenic vein thrombosis and nocirrhosis, and 10 cirrhotic patients without thrombosis. The splenic pressure was measured by percu-taneous puncture below the curvature of the ribs with an angle of the needle to skin of 30° in order tominimize the risk of cutting the spleen if the patient took a deep breath.Results: None of the patients inwhom the described procedure was followed had complications. Pressure measurements in the spleenpulp and splenic vein were concordant. The pressure gradient across the portal venous system (splenic-to-wedged hepatic vein pressure) was�1.3 to 8.5 mmHg (median, 2.8 mmHg) in cirrhosis patients and0–44 mmHg (median, 18 mmHg) in thrombosis patients, the variation reflecting various degrees ofobstruction to flow in the portal venous system. Peripheral portal pressure (splenic-to-free liver veinpressure gradient) was 1.1–28 mmHg (median, 17 mmHg) in cirrhotic patients and 11–52 mmHg(median, 23 mmHg) in thrombosis patients.Conclusions: Liver vein catheterization combined withpercutaneous splenic pressure measurement is feasible in quantifying pressure gradient across a throm-bosis of the portal/splenic vein and in quantifying portal pressure peripheral to this kind of thrombosis.
Key words: Liver cirrhosis; oesophageal varices; portal hypertension; splanchnic haemodynamics
Susanne Keiding, M.D., Dept. of Medicine V, Aarhus University Hospital, DK 8000 Aarhus, Denmark(fax. �45 8949 3020, e-mail. [email protected])
Patients with thrombosis of the portal or the splenic veinmay develop portal hypertension that is often com-plicated by gastric or oesophageal varices with bleed-
ing (1). Diagnosis is based on ultrasound or CT scanning (2)but without quantification of the portal pressure of importancefor the risk of variceal bleeding. In cirrhosis, the portal venouspressure is routinely measured indirectly during liver veincatheterization, with the catheter in a wedged position; a null-reference is the pressure measurement with the catheter in afree position (3–6). Portal venous pressure can be measureddirectly by percutaneous puncture of the portal vein, by thepercutaneous transhepatic approach (7–12) or via catheteriza-tion of the umbilical vein (9) but these methods are biased bylack of a proper null-reference measurement. Ultrasound-guided puncture of the portal vein from a hepatic vein duringthe transjugular intrahepatic portosystemic stent-shunt (TIPS)procedure is the only method today that includes pressuremeasurements directly in the portal vein and in a free livervein (14). These techniques cannot, however, measure thepathophysiologically relevant portal pressure of patients with
thrombosis of the portal or splenic vein, because theobstruction to the blood flow is peripheral to the accessiblepart of the portal venous system. Around 30–40 years agoradiological studies were widely used to assess the anatomy ofthe portal venous system of patients with thrombotic diseases.In 1986 Burchardt et al. (15) combined percutaneous spleno-portography and percutaneous transhepatic portography forthe assessment of thrombosis of the portal venous system withpressure measurements. This procedure measures the gradientacross the thrombosis but not the portal pressure of relevancefor the risk of variceal bleeding, namely the portal pressureperipheral to the thrombosis. We, therefore, undertook thepresent prospective study of patients with and withoutthrombosis in the portal and/or splenic vein to examine thefeasibility of combined pressure measurement by liver veincatheterization and percutaneous puncture of the spleen. Thepurpose was to examine the feasibility of measurements of 1)the pressure gradient across the thrombosis, if any, and 2) theportal pressure peripherally to the obstruction of the bloodflow with reference to the pressure in the free liver vein.
ORIGINAL ARTICLE
2004 Taylor & Francis DOI 10.1080/00365520410005171
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Patients and Methods
PatientsTwenty-one patients were consecutively included in the
study. Eleven patients had thrombosis of the portal venoussystem and no cirrhosis and 10 patients had liver cirrhosiswithout thrombosis. Data from the only patient where thesplenic pressure could not be measured because of technicalproblems are not included in the material. The material thusconsists of paired pressure measurements in the hepatic veinand the spleen in 20 patients. The patients gave writteninformed consent to the procedures. The Ethics Committee ofAarhus County approved the study.
In the group of 10 patients (9 M, 1 F) with thrombosis, 7patients had thrombosis of the portal vein, 2 patients hadthrombosis of the splenic vein, and 1 patient of both vessels.The aetiology of the thrombosis was related to primarydisease of the coagulation system in 4 patients, severe pan-creatitis in 3 patients, sequelae after catheterization of theumbilical vein as a premature child in 1 patient, and unknownin 2 patients. The clinical index symptom was bleeding fromoesophageal varices in 3 patients, bleeding from gastricvarices in 1 patient, abdominal pain in 5 patients, andthrombocytopenia in 1 patient. The aetiologies and presentingsymptoms were similar to those in other studies (2). At thetime of the study, 7 patients had oesophageal varices alone, 2patients had varices in the gastric fundus alone, and 1 patienthad varices at both locations. Four patients had bled withinthe preceding 3 months. Age was 24–71 years (median 34years). In the group of 10 (8 M, 2 F) liver cirrhosis patientswith no venous thrombosis, the aetiology was alcoholiccirrhosis in 7 cases, autoimmune cirrhosis in 1 case, andcryptogenic cirrhosis in 2 cases. Every patient had oesopha-geal varices, none had gastric varices; 3 patients had bledwithin the preceding 3 months. Age was 30–58 years (median51 years).
Pre-study clinical examinationsThe patients underwent routine clinical examinations,
including interviews, physical examination, histology of aliver biopsy and standard blood tests. The thrombosis wasdiagnosed by Doppler ultrasound examination and CTscanning. Plasma albumin ranged from 343 to 618�mol/L(median, 582�mol/L) in cirrhotic patients and from 548 to649�mol/L (median, 606�mol/L) in non-cirrhotic patients.Reference values in our laboratory for healthy controls are551–725�mol/L. The galactose elimination capacity (16, 17)was 16–50�mol min�1 kg�1 (median, 23�mol min�1 kg�1)in cirrhosis patients and 17–43�mol min�1 kg�1 (median,28�mol min�1 kg�1) in non-cirrhosis patients. Referencevalues in healthy controls are 20–40�mol min�1 kg�1
(median, 32�mol min�1 kg�1) (18).
Hepatic vein catheterizationThis procedure has been described in detail previously (5).
In short, the patients were fasted overnight. If requested by thepatient, 5 mg benzodiazepine was given orally (diazepam,Dumex-Alpharma, Copenhagen, Denmark) or intravenously(midazolam, Dumex-Alpharma, Copenhagen, Denmark). Thepatient was in supine position during the measurementprocedures. A liver vein catheter of the Cournand type, i.e.with a hole in the tip and no side holes or balloon (RadiopaquePolyethylene Catheter, curve DK.B.10, 6.7 F; Cook, Bjae-verskov, Denmark) was introduced through an introducercatheter placed percutaneously in the right femoral vein. Thecatheter tip was advanced into a ‘wedged position’ in one ofthe right liver veins by means of a guidewire and underfluoroscopy. Each wedged position of the tip of the catheterwas verified by injection of X-ray-contrast (Omnipaque240 mg/mL; Nycomed DAK, Roskilde, Denmark). Thepressure was recorded (Quadriscope 8041; Simonsen &Weel, Albertslund, Denmark) 10 times within 2 min. Subse-quently, the catheter was retracted to the ‘free position’ in theliver vein, and the pressure was recorded 10 times. Thewedged-to-free hepatic venous pressure gradient was calcu-lated as the difference between the mean values. Themeasurements were repeated in 2–3 separate veins becauseof the segmental variation of pressure gradients in thecirrhotic liver. The highest pressure, which determines therisk of variceal bleeding (5), was used in the present study.
Spleen pressureThe splenic pressure was measured 15–60 min after
completion of the liver vein catheterization procedures. Thepatient lay on the right side with the left arm over his/herhead. The localization and size of the spleen and its vesselswere visualized by ultrasound examination (Tosbee Ultra-sound Scanner SSA-240A, Toshiba Medical Systems, Japan)using a 3.75 MHz transducer. The site of the percutaneouspuncture was chosen just below the left curvature of the ribs.Local anaesthesia (Lidocain, 10 mg/mL, 5 mL; DanishHospitals’ Pharmacy, Copenhagen) was injected into theskin and the peritoneum at the puncture site. The patient wasasked to hold his/her breath for 20–30 s, and a 12-cm-longneedle, diameter 0.9 mm (20 G) (Mediplast, Japan), con-nected to the pressure recording system (see above) wasintroduced into the spleen at a 30°angle from the skin surface.During ultrasonic guidance, the needle was advanced into thespleen so that the tip was located in the central part of theparenchyma, and the pressure was recorded 5–8 times. In 12patients the tip of the needle was then advanced into anintrasplenic vein and the pressure recorded 5–8 times. Themean pressures were used, corrected for differences in thehydrostatic pressures during the measurements in the spleenand the liver vein, ranging from 3 to 9 mmHg, and measuredwith the tip of the needle in the air at the level of the spleen,when the patient was lying on the right side and on the back,respectively.
The reason for using the needle at a 30° angle to the skinwas to minimize the risk of cutting the spleen and thus to
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prevent the risk of bleeding. If a patient took a deep breathwith the needle within the spleen, the spleen would movealong the longitudinal direction of the needle and the damageto the spleen would be less than if the needle had beenintroduced at, for example, an angle of 90°.
Results
Pressure measurementsIn Fig. 1 it is shown that the pressure measurements in the
splenic vein and the splenic parenchyma correlated well inboth patients with and without thrombosis of the portalvenous system. The splenic parenchyma-to-splenic veinpressure difference ranged from�4.8 to 9.1 mmHg (median,0.6 mmHg;n = 12). The average difference was not signifi-
cantly different from zero (pairedt test, P � 0.3) but thevariation was larger than the technical measurement uncer-tainty of 1–2 mmHg (5).
The pressure gradient across the portal venous system wasmeasured as the difference between the pressures in thesplenic parenchyma and the wedged liver vein position. In thegroup of cirrhotic patients (without thrombosis) the gradientranged from�1.3 to 8.5 mmHg (Table I). The averagegradient was 2.9 mmHg and the 95% confidence limits 3.3 to9.1 mmHg. In the group of patients with thrombosis of theportal venous system, the splenic-to-wedged pressure gradi-ent ranged from 0 to 44 mmHg (Table I). The median gradientin thrombotic patients (18 mmHg) was significantly higherthan that of the non-thrombotic patients (2.9 mmHg) (TableI). The Doppler ultrasound examination showed recanaliza-tion of the thrombosis and/or cavernous collaterals in threepatients with pressure gradients within the reference interval.In the remaining cases there was no definitive correlationbetween the pressure gradient and the degree of obstruction asdetermined by ultrasound or CT.
The peripheral portal pressure, measured as the splenic-to-free liver vein pressure gradient, was equal to or higher than11 mmHg in each thrombotic case. The median value(23 mmHg) was significantly higher in this group of patientsthan in the group of cirrhotics without thrombosis (17 mmHg)(Table I). In Fig. 2 we present the frequency distribution ofthe peripheral portal pressure with indications of whether ornot the patient had bled from varices within the preceding 3months. The pressures in patients with variceal bleeding weresimilar in the two groups of patients. The relation between thepressure gradient across the portal vein and the peripheralportal pressure (Fig. 3) shows no significant correlation forthe group without thrombosis, whereas there was a tendencytowards a positive correlation for patients with thrombosis.
Side effectsOne patient had minor complaints owing to transient
thrombosis of the femoral vein after the liver vein catheter-ization procedure. No other complication attributable to thispart of the procedures was seen. None of the patients, inwhom the described spleen puncture procedure was followed,
Fig. 1. Relation between pressure measurements in the splenicparenchyma and a splenic vein in 6 patients with thrombosis of theportal vein and/or the splenic vein and without liver cirrhosis (�)and in 6 cirrhotic patients without thrombosis (�). The line ofidentity is shown.
Table I. Pressure measurements in the spleen and liver vein in patients with and without thrombosis of the portal venous system
Cirrhotic patientswithout thrombosis
Non-cirrhotic patients withthrombosis of the portal
and/or splenic vein
Number of patients 10 10Hepatic wedged-to-free pressure gradient1, mmHg 1.8–25 (13) 0.8–20 (7.1)Pressure gradient across the portal venous system (splenic-to-wedged liver vein
pressure gradient), mmHg�1.3–8.5 (2.9) 0–44 (18)
Peripheral portal vein pressure (splenic-to-free liver vein pressure difference),mmHg
1.1–28 (17) 11–52 (23)
Continuous variables are given as range (median).1Equal to HVPG (hepatic venous pressure gradient) for patients without thrombosis of the portal venous system.Controls:�6.7 mmHg (Ref. 5).
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experienced any adverse side effects. In 2 patients the needlewas introduced between the lower ribs and at an approxi-mately 90° angle to the body surface; both had complicationsof the procedures. One patient had pain in the abdomen forapproximately one hour but without changes in bloodpressure or pulse rate. No specific treatment was required.Ultrasound examination the following day showed a smallhaematoma in the splenic pulp. Another patient developedsevere abdominal pain and low blood pressure. Ultrasoundexamination showed bleeding from the spleen. An artery tothat part of the spleen was embolized during ultrasoundscanning and the patient recovered within a few days. None ofthe patients experienced long-term adverse side effects.
Discussion
The study shows that it is safe and feasible to quantify thepressure gradient across a thrombosis in the portal venoussystem and the pressure peripheral to the thrombosis bycombined percutaneous splenic pressure measurement andliver vein catheterization.
The pressure measurements in the splenic parenchyma anda splenic vein showed good agreement (Fig. 1). The punctureof a splenic vein can be technically difficult and carries ahigher risk than puncture of the parenchyma. It is thereforeadvantageous that pressure measurement in the splenicparenchyma can replace measurement in a splenic vein.
In cirrhotic patients without thrombosis, the splenic-to-wedged liver vein pressure gradient was on average2.9 mmHg. The variation was small and it did not correlateto the portal vein pressure (Fig. 3). It reflects the pathophy-siological pressure gradient along the blood flow in the portalvein with no thrombosis, including possible temporal fluc-tuation in the time interval of up to 60 min between the twomeasurement procedures. These findings validate the use ofthe wedged liver vein pressure as an indirect measure of theportal vein pressure in non-thrombotic patients and confirmthe results found in cirrhosis by others (7–12).
In patients with thrombosis, the splenic-to-wedged liver
Fig. 3. Relation between the pressure gradient across the portal vein(i.e. splenic-to-wedged liver vein pressure gradient) and theperipheral portal pressure (i.e. splenic parenchyma pressure minusthe free liver vein pressure) in 10 patients with thrombosis of theportal vein and/or the splenic vein (�) and 10 patients withoutthrombosis (�). In the group of patients without thrombosis, thegradient across the portal vein was on average 2.9� 3.1 mmHg (�s(standard deviation)). The figure shows the line of this average value(�) and lines of the 95% confidence intervals, i.e.�2.7 to8.9 mmHg.
Fig. 2. Frequency distribution of the peripheral portal pressure incirrhotic patients without thrombosis (top panel) and in non-cirrhoticpatients with thrombosis of the portal and/or the splenic vein (lowerpanel). The peripheral portal pressure was calculated as the pressuremeasured in the splenic parenchyma, corrected for a null-referencepressure measured in the free catheter position in the liver vein. Datafrom patients who had bled within the preceding 3 months areindicated (�).
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vein pressure gradient varied markedly (Table I and Fig. 3).This reflects the haemodynamic effects of varying degrees ofobstruction to the flow by the thrombotic occlusion of thevein, in agreement with the study by Burchardt et al. (15). Thelack of correlation between the pressure gradient and thedegree of recanalization of the portal venous thrombosis orcollateral vessels as assessed by Doppler ultrasound and CTmay be due to the well-known limitations of these imagingtechniques, even by a trained examiner, of deciding defini-tively the degree of occlusion by portal or splenic venousthrombosis. These results underline the importance of com-bining morphological assessment of a thrombosis by imagingtechniques with quantification of the pressures of pathophy-siological importance.
The relevant pressure for the risk of variceal bleeding is theportal pressure peripheral to the occlusion site, measured withan appropriate null-reference pressure measurement such asthat in the free liver vein. The frequency of variceal bleedingand relation to the portal pressure in the present small groupof cirrhotics (Fig. 2) is the same as that in larger materials (5).The similar bleeding frequency and the similar relation to theperipheral portal pressure for the two groups of patientsindicate that the pressure carrying an increased risk ofbleeding is of the same order of magnitude in thromboticpatients as in cirrhotic patients. It is worth mentioning that thepatient with the peripheral portal pressure of 52 mmHg hadsevere chronic pancreatitis, total thrombotic occlusion of boththe portal and the splenic vein with cavernous collaterals andmonstrous oesophageal and gastric varices; yet he had notexperienced any bleeding episodes.
The wedged-to-free pressure gradient in the cirrhotics(Table I) was within the range usually seen in this group ofpatients (5). Approximately half of the patients withthrombosis had higher gradients than the values in patientswithout liver disease (Table I), reflecting that some of thepatients had liver fibrosis or sequelae to gallstones.
The present percutaneous procedure of measuring thesplenic pressures seems feasible since it is without adverseside effects provided the described technique is strictlyadhered to. We saw adverse side effects only in the twopatients in whom this was not done. In fact, each of the otherpatients reported less discomfort by the pressure measure-ments in spleen than by the liver vein catheterizationprocedure. Misra et al. (19) saw local pain and tendernessin 33% and subcapsular haematoma in 7% of 45 non-cirrhoticpatients after splenoportovenography, and Sawada et al. (20)report that 1 of 10 patients experienced discomfort due tosubcapsular contrast accumulation following percutaneoustranssplenic portography. Other investigators (11, 15) do notmention any side effects. None of the quoted papers mentionwhich angle of the needle to the skin was used.
We conclude that combined liver vein catheterization andpercutaneous splenic pressure measurement is safe andfeasible for quantification of the pressure gradient across athrombosis of the portal or splenic vein and the portal pressure
peripheral to this kind of thrombosis. We must urge the use ofpercutaneous puncture below the curvature of the ribs and anangle of the needle to the skin of approximately 30° in orderto minimize the risk of a cut in the spleen if the patient takes adeep breath during the procedure. As far as we know, there areno studies of the importance of the peripheral portal pressurefor the risk of the development of oesophageal or gastricvarices, risk of bleeding or response to medical treatment.Furthermore, there are no studies of the effect of medicaltreatment of the peripheral portal pressure. The low risk ofthese procedures sets the scene for clinical studies of suchquestions.
Acknowledgements
We thank Gunhild Brandt Andersen and Inger Schiøtt forexcellent technical assistance.
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Received 18 August 2003Accepted 26 January 2004
Note added in proof
Illustration of the pressure gradients and two typical positionsof a thrombosis in the portal vein. Pressurea is measured inthe free liver vein position; pressureb in the wedged liver veinposition; and pressurec in the splenic parenchyma. Pressuregradients: (b–a) = hepatic venous pressure gradient, HVPG(mmHg); (c–b) = pressure gradient across portal venoussystem (mmHg); and (c–a) = peripheral portal pressure(mmHg).
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