Influence of the Spleen on Portal Haemodynamics: a Non-invasive Study with Doppler Ultrasound in Chronic Liver Disease and Haematological Disorders

Background: Splanchnic haemodynamic parameters for the differential diagnosis of splenomegalies of different origins are still suboptimal and the role of spleen enlargement in cirrhosis remains controversial. In an attempt to elucidate these questions, we assessed splanchnic haemodynamics in chronic liver diseases and various other disorders with splenomegaly. Methods: Study groups comprised: (i) patients with chronic liver disease (89 with cirrhosis, 35 with chronic hepatitis), (ii) patients with splenomegaly without relevant portal hypertension (14 with haematological splenomegaly and 25 liver transplant recipients without complications), (iii) 15 patients with arterial hypertension, (iv) 22 healthy controls. In all subjects, spleen size, portal flow parameters and splenic artery resistance index were measured using duplex-Doppler ultrasound. Results: Splenic artery resistance index was significantly and selectively increased in patients with cirrhosis (0.63, whereas all other group means ranged between 0.53 and 0.56; P < 0.01). Portal flow velocity was significantly decreased in cirrhosis ( P < 0.01). The combination of these two parameters provided an accuracy of 87.5% in distinguishing portal hypertensive from haematological splenomegaly. In patients with cirrhosis, the degree of spleen enlargement was positively correlated with increasing portal flow volume, portal vein diameter and variceal size, whereas splenic resistance index and portal velocity did not differ in connection with spleen size. Conclusions: Splenoportal Doppler sonography provides specific findings in cirrhosis and may therefore be a useful tool in differentiating between splenomegaly of portal hypertensive or haematological origin. In patients with cirrhosis, the presence of splenomegaly is associated with the presence of larger oesophageal varices.     

Differences in Portal Hemodynamics in Cirrhosis and Idiopathic Portal Hypertension

A comparative study of portal hemodynamics was made in 79 cirrhotics (24 cirrhotics with a large spleen greater than or equal to 500 cm3 in volume, 55 cirrhotics with a spleen less than 500 cm3 in volume), 22 patients with idiopathic portal hypertension, and 63 healthy adults who served as the control for portal and splenic venous flows. Portal and splenic venous flows were significantly increased in the group order of the cirrhosis without splenomegaly group, the cirrhosis with splenomegaly group, and idiopathic portal hypertension group. Intrahepatic shunt index was significantly greater in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly group, and it was negligible in the idiopathic portal hypertension group. Portal vein pressure was significantly elevated in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly and idiopathic portal hypertension groups. Postsinusoidal resistances were significantly greater in the two groups of cirrhosis than in the idiopathic portal hypertension group, whereas presinusoidal resistance was significantly greater in the idiopathic portal hypertension group than in the two groups with cirrhosis. It is concluded that these differences are inconsistent with the view that cirrhosis with splenomegaly comes from idiopathic portal hypertension.     

Ultrasonography in patients with chronic liver disease: its usefulness in the diagnosis of cirrhosis.

OBJECTIVE: To prospectively assess the usefulness of ultrasonography in predicting the presence of cirrhosis in patients with asymptomatic chronic liver disease in unknown stage. EXPERIMENTAL DESIGN: Eighteen doppler and ultrasonographic features were prospectively assessed immediately before performing laparoscopy and/or liver biopsy. Usefulness of predictive variables selected by multiple regression analysis and included in a scoring scale was determined by ROC curves. PATIENTS: One hundred and thirteen consecutive patients with neither clinical nor biochemical signs of advanced liver disease submitted for study. RESULTS: Liver enlargement, liver surface nodularity, liver parenchyma distortion, flattening of flow wave in hepatic veins, portal and splenic veins dilatation, decreased variability in splenic vein caliber with breathing. Collateral vessels, and splenomegaly were associated to cirrhosis. Multivariate analysis showed the joint assessment of hepatic echostructure, portal vein caliber and spleen area to be the best approach to ultrasonographic staging, with sensitivity of 80%, specificity of 92% and accuracy of 89% in the diagnosis of cirrhosis. CONCLUSIONS: Ultrasonography enabled the presence or absence of cirrhosis to be correctly determined even in patients with asymptomatic disease. Combined assessment of hepatic echostructure, portal vein diameter and spleen size provides the highest accuracy.     

Role of spleen enlargement in cirrhosis with portal hypertension

The possible relationships between splenomegaly and portal hypertension have been analysed in patients with cirrhosis. In this condition, splenomegaly is not only caused by portal congestion, but it is mainly due to tissue hyperplasia and fibrosis. The increase in spleen size is followed by an increase in splenic blood flow, which participates in portal hypertension actively congesting the portal system.     

Portal hemodynamics as predictors of high risk esophageal varices in cirrhotic patients

AIM： To evaluate portal hypertension parameters in liver cirrhosis patients with and without esophageal varices （EV）. METHODS： A cohort of patients with biopsy confirmed liver cirrhosis was investigated endoscopically and with color Doppler ultrasonography as a possible noninvasive predictive tool. The relationship between portal hemodynamics and the presence and size of EV was evaluated using uni- and multivariate approaches. RESULTS： Eighty five consecutive cirrhotic patients （43 men and 42 women） were enrolled. Mean age （± SD） was 47.5 （± 15.9）. Portal vein diameter （13.88 ± 2.42 vs 12.00 ± 1.69, P 〈 0.0005） and liver vascular index （8.31 ± 2.72 vs 17.8 ± 6.28, P 〈 0.0005） were found to be significantly higher in patients with EV irrespective of size and in patients with large varices （14.54 ± 1.48 vs 13.24 ± 2.55, P 〈 0.05 and 6.45 ± 2.78 v$10.96 ± 5.05, P 〈 0.0005, respectively）, while portal vein flow velocity （13.25 ± 3.66 vs 20.25 ± 5.05, P 〈 0.0005）, congestion index （CI） （0.11 ± 0.03 vs 0.06 ± 0.03, P 〈 0.0005）, portal hypertensive index （2.62 ± 0.79 vs 1.33 ± 0.53, P 〈 0.0005）, and hepatic （0.73 ± 0.07 vs 0.66 ± 0.07, P 〈 0.001） and splenic artery resistance index （R/） （0.73 ± 0.06 vs 0.62 ± 0.08, P 〈 0.0005） were significantly lower. A logistic regression model confirmed spleen size （P = 0.002, AUC 0.72） and portal hypertensive index （P = 0.040, AUC 0.79） as independent predictors for the occurrence of large esophageal varices （LEV）. CONCLUSION： Our data suggest two independent situations for beginning endoscopic evaluation of compensated cirrhotic patients： Portal hypertensive index 〉 2.08 and spleen size 〉 15.05 cm. These factors may help identifying patients with a low probability of LEV who may not need upper gastrointestinal endoscopy.     

Reticuloendothelial Phagocytic Function in Human Liver Disease and its Relationship to Haemolysis

Summary . This study was undertaken to examine the hypothesis that enhanced reticuloendothelial (RE) phagocytosis and splenic sequestration of red blood cells are important aetiological factors in the haemolysis accompanying liver disease. RE phagocytic capacity (REPC) was measured by the rate of plasma disappearance of radio-iodinated microaggregated human serum albumin (¹²⁵I-MAA) in 57 patients with acute or chronic liver disease, and its relationship to splenic size, RBC survival and splenic sequestration of RBC was analysed. In addition, RE perfusion was measured using a tracer dose of ¹²⁵I-MAA, and the RE phagocytic index (REPI), an index of the individual cellular RE activity, independent of perfusion, was calculated. An increased REPI was found in all forms of liver disease, largely independent of aetiology or severity. REPC was normal in most forms of cirrhosis but was decreased in patients with alcoholic cirrhosis, many of whom had diminished RE perfusion, associated with clinical or radiographic evidence of portal systemic shunting. This decreased REPC was due to decreased RE perfusion since a close correlation between REPC and RE perfusion was demonstrated. The relationship between spleen size and REPC in patients with cirrhosis depended on the aetiology of the disease, since in alcoholic cirrhosis splenomegaly was usually indicative of portal hypertension, whereas in patients with active chronic hepatitis splenomegaly was often an integral part of the disease. A shortened RBC survival was demonstrated in 24 of 30 patients studied, but the degree of haemolysis did not correlate with REPC, REPI or splenic size. Furthermore, splenic sequestration of RBC could be demonstrated in only two patients. It would appear that in hepatic cirrhosis, the RE system, whether its phagocytic capacity is increased or decreased, removes effete RBC presented to it, but is not primarily responsible for the mild haemolytic process.     

Significance of Enhanced Expression of Nitric Oxide Syntheses in Splenic Sinus Lining Cells in Altered Portal Hemodynamics of Idiopathic Portal Hypertension

Idiopathic portal hypertension (IPH) is characterized by noncirrhotic portal hypertension due mainly to increased intrahepatic, presinusoidal resistance to portal blood flow. Marked splenomegaly is always seen in IPH. To clarify the pathogenetic significance of splenomegaly, immunohistochemical expression of inducible nitric oxide synthese (iNOS), endothelial NOS (eNOS), and endothelin-1 (ET-1) in spleens from patients with IPH was examined. Sinus lining cells of IPH spleens showed diffuse and strong expression of iNOS and eNOS. Sinus lining cells of spleens from patients with liver cirrhosis (LC) also showed positive signals for iNOS and eNOS, but the staining intensity was significantly weak. ET-1 was detectable in only a few mononuclear leukocytes in the red pulp of both IPH and LC spleens. These results suggest that NO liberated in spleen, rather than ET-1, is responsible for the dilatation of splenic sinuses, leading to splenomegaly, and thereby contributes to portal hypertension in IPH.     

Effect of somatostatin on splanchnic hemodynamics in patients with liver cirrhosis and portal hypertension

The effect of somatostatin on splanchnic hemodynamics in patients with liver cirrhosis is not clearly defined, as some authors report a decrease in portal pressure and in liver blood flow during intravenous administration of this hormone, while others do not. In 19 subjects with liver cirrhosis and portal hypertension the following parameters were measured before and during intravenous administration of somatostatin (7.5 micrograms/min): porto-hepatic gradient, estimated hepatic blood flow, specific splenic blood flow, cardiac index. Estimated hepatic blood flow decreased significantly during somatostatin infusion (p less than 0.05), averaging a 13% decrease; porto-hepatic gradient, splenic specific blood flow and cardiac index did not vary significantly. These data indicate that somatostatin infused at a dose of 7.5 micrograms/min induces a slight decrease in liver blood flow without affecting portal hypertension.     

Noninvasive Prediction of Large Esophageal Varices in Chronic Liver Disease Patients

Background/Aim:

Esophageal varices (EVs) are a serious consequence of portal hypertension in patients with liver diseases. Several studies have evaluated possible noninvasive markers of EVs to reduce the number of unnecessary endoscopies in patients with cirrhosis but without varices. This prospective study was conducted to evaluate noninvasive predictors of large varices (LV).

Patients and Methods:

The study analyzed 106 patients with liver diseases from January 2007 to March 2008. Relevant clinical parameters assessed included Child-Pugh class, ascites and splenomegaly. Laboratory parameters like hemoglobin level, platelet count, prothrombin time, serum bilirubin, albumin and ultrasonographic characteristics like splenic size, splenic vein size, portal vein diameter were assessed. Univariate and multivariate analysis was done on the data for predictors of large EVs.

Results:

Incidence of large varices was seen in 41%. On multivariate analysis, independent predictors for the presence of LV were palpable spleen, low platelet count, spleen size >13.8 mm, portal vein >13 mm, splenic vein >11.5 mm. The receiver operating characteristic (ROC) curve showed 0.883 area under curve. Platelet spleen diameter ratio 909 had a sensitivity and specificity of 88.5%, 83% respectively.

Conclusion:

Thrombocytopenia, large spleen size, portal vein size and platelet spleen diameter ratio strongly predicts large number of EVs.     

Diagnostic value of Doppler assessment of the hepatic and portal vessels and ultrasound of the spleen in liver disease

OBJECTIVES: To investigate the clinical utility and the intra-observer and inter-observer variability of Doppler ultrasound assessment of the hepatic and portal vessels along with measurement of spleen size in the diagnosis of chronic liver disease and cirrhosis. METHODS AND MATERIALS: Ultrasound measurements of portal vein diameter (PVD), portal vein velocity (PVV), hepatic arterial resistance index (HARI), hepatic vein profile (HVP), and spleen size were obtained in 49 controls and 45 patients with liver disease (23 with primary biliary cirrhosis, 22 with hepatitis C) by two experienced observers, who each performed three blinded measurements of each variable. Control values were derived from normal hospital workers. Percutaneous liver biopsies in 41 of the patients showed cirrhosis (14 patients), moderate/severe fibrosis (13 patients), and early disease (14 patients). RESULTS: Seventy-one percent of cirrhotic patients had splenomegaly (> 13.6 cm). The spleen size was significantly larger in cirrhotics (16.0 cm) than in non-cirrhotics (13.0 cm, P < 0.009) and healthy controls (10.7 cm, P < 0.00005), and was the only independent predictor of cirrhosis, with a threshold of 15 cm predicting cirrhosis with a specificity of 98%, positive predictive value of 93%, sensitivity of 57% and negative predictive value of 80%. HVP was abnormal in 76.9% of cirrhotics, 57.7% of non-cirrhotics and 2.1% of controls (P < 0.04). However, the mean PVV, PVD and HARI were no different between controls and patients or between cirrhotic and non-cirrhotic liver disease. There was significant inter-observer variability for PVV, but intra-observer and inter-observer variability was acceptable for the other measurements. CONCLUSIONS: Splenomegaly size and abnormal HVP are useful predictors of chronic liver disease and cirrhosis, and both can be measured reliably and reproducibly. However, Doppler measurements of PVV, PVD and HARI are not useful in distinguishing patients with chronic liver disease from normal controls.     

Portal Hypertension and Esophageal Varices in Cystic Fibrosis: Unreliability of Echo-Doppler Flowmetry

To investigate the role of echo-Doppler flowmetry in evaluating patients with cystic fibrosis and portal hypertension at risk of esophageal varices, we studied 26 subjects divided in 3 groups: 9 with portal hypertension and esophageal varices, 8 with chronic liver disease without varices, and 9 without chronic liver disease. Spleen size, diameter, blood velocity, and flow rate of portal, splenic, and superior mesenteric veins were recorded. In patients without chronic liver disease Doppler measurements were repeated on 2 different days to assess intraobserver variability. Significant differences among the three groups were found for mean values of spleen size and diameters of portal, splenic, and superior mesenteric veins. Nevertheless, a considerable overlapping of individual data was observed. No differences were observed in mean hemodynamic measurements, except for blood velocity in portal vein and flow rate in splenic vein. The intraobserver variability for repeated Doppler measurements was clinically unacceptable for most of the variables studied. Echo-Doppler assessment of splanchnic flow seems to be an unreliable tool in the management of cystic fibrosis patients with portal hypertension at risk of esophageal varices.     

Portal hemodynamics in idiopathic portal hypertension (Banti's syndrome). Comparison with chronic persistent hepatitis and normal subjects

A comparative study of portal hemodynamics was made in 17 patients with idiopathic portal hypertension, 5 patients with chronic persistent hepatitis having no portal hypertension, and 21 healthy adults who served as the control for certain measurements. Venous pressures were measured by portal and hepatic vein catheterizations, blood flow by the pulsed Doppler flowmeter, organ volume by computed tomography, and intrahepatic shunt index by 99mTc-macroaggregated albumin instilled in the portal vein. The patients with idiopathic portal hypertension were divided into two groups: group A (n = 8) and group B (n = 9), consisting of those who respectively had portal venous flow per liver volume above and below the mean + 2 SD of healthy adults. In group A, portal vein pressure was moderately elevated, portal venous flow was significantly increased compared with the control, and portal vascular resistance was not much altered. In group B, portal vein pressure was markedly elevated above that of control, portal venous flow was comparable, and portal vascular resistance was significantly elevated. Splenic venous flow measured in the splenic vein between the left and short gastric veins was markedly increased in groups A and B, the increase being greater in the former. It was concluded that in some patients with idiopathic portal hypertension, increased portal venous flow, partly a result of increased splenic venous flow secondary to splenomegaly of an undetermined process, is the main contributor initially to the elevation of portal vein pressure; in others, possibly later, increased portal vascular resistance plays an important role.     

Doppler hemodynamic study in portal hypertension and hepatic encephalopathy

BACKGROUND/AIMS: The aim of our study was to evaluate and compare the differences in the parameters of portal hypertension in two groups of patients with liver cirrhosis, with and without hepatic encephalopathy (HE). METHODOLOGY: 30 patients with liver cirrhosis, 17 (56.7%) of them with HE, were investigated by clinical, neurological, laboratory, endoscopic methods and with color Doppler ultrasonography (CDU) at the Institute for Digestive Diseases, Clinical Center of Serbia, Beograde. RESULTS: Significant correlation was found between the diameters of the right liver lobe and the portal vein (p=0.01), and also between the diameters of the spleen and splenic vein (p=0.0002), in both groups of patients. Mean portal vein diameter significantly increases (p=0.01) in patients with HE (14.87 +/- 1.86mm), compared to those without HE (13.2 +/- 2.31mm), while mean splenic vein diameter was not significantly different in the two groups. In patients with ascites, CDU showed significantly lower (p=0.03) portal flow velocity (11.87 +/- 6.25cm/ sec), compared to those without ascites (14.33 +/- 4.41cm/sec). Splenic flow velocity was not significantly different (16.00 +/- 6.60cm/sec with ascites and 14.61 +/- 5.29cm/sec without ascites). In patients with HE, portal flow velocity was significantly lower (9.00 +/- 5.41cm/sec) compared to those without HE (14.0 +/- 7.03cm/sec) (p=0.04). Mean splenic flow velocity was significantly lower (p=0.03) in patients with HE (12.60 +/- 4.16cm/sec), compared to those without HE (17.77 +/- 5.91cm/sec). Portal flow velocity shows linear decrease, related to the increase of the liver damage (Child-Pugh score), while splenic velocity was not related to this parameter. CONCLUSIONS: Ultrasonographic parameters of portal hypertension show significant correlation between the diameters of liver/portal vein and spleen/splenic vein. Portal hemodynamic parameter (blood flow velocity) is significantly related to the stages of liver damage, presence of ascites and HE, while splenic hemodynamics is specific and not directly related to these parameters.     

Splenomegaly—an insensitive sign of portal hypertension

The prevalence of splenomegaly associated with portal hypertension was examined in a consecutive population of III patients who had portal hypertension diagnosed using specific endoscopie, sonographic, and Doppler signs. Splenic size was measured objectively via its cranio-caudal length on coronal section using ultrasound and by clinical examination. Sonographically, 52% of patients had a definitely large spleen and 35% a spleen less than one standard deviation from the normal mean, while a further 13% had equivocal splenomegaly. Only 52% of patients had splenomegaly on clinical assessment. Splenomegaly was less common in patients with alcoholic (41% definite, 15% equivocal) than in those with non-alcoholic liver disease (66% definite, 17% equivocal, p= 0.02) and splenic length was significantly smaller in alcoholic patients (12.7±0.5cm) compared to patients with either non-alcoholic liver disease (15.0±0.6cm, p= 0.003) or portal hypertension due to vascular occlusive diseases (16.5 ± 2.0 cm, p= 0.006). Splenomegaly, whether assessed sonographically or clinically, is an insensitive sign of portal hypertension and its absence cannot be used as a negative predictor of the presence of portal hypertension in patients with chronic liver disease.     

''Non-Tropical Idiopathic Splenomegaly'' (''Primary Hypersplenism''): A Review of Ten Cases and their Relationship to Malignant Lymphomas

Summary . The clinical, haematological and serological findings arc described of 10 patients believed to be suffering from a syndrome tentatively labelled ‘non-tropical idiopathic splenomegaly’. The blood picture was characterized by leucopenia and neutropenia of severe degree, moderate thrombocytopenia and slight to moderate reticulocytosis. Abnormal or early forms of leucocytes were absent from peripheral blood films. All the patients were anaemic, although in only two was the total red-cell volume subnormal. Five developed auto-antibodies against red cells; one had hypogammaglobulinaemia. The spleen was grossly enlarged in all 10 patients and the liver was palpable in seven but there was no evidence of cirrhosis or portal hypertension. Splenectomy was carried out in nine of the patients, with sustained and striking clinical and haematological improvement in most instances. Four patients, however, remained neutropenic. The histological findings in the spleens were variable and in some of the patients the lymphoid foci were enlarged. There was, however, no evidence of overt malignant lymphoma. Four of the patients have died: two from illnesses unconnected with their splenomegaly; one from lymphosarcoma 8 months after splenectomy and one from auto-immune haemolytic anaemia 4¹/₂ years after splenectomy—this patient also showed evidence of lymphosarcoma at necropsy. The nature of the splenic enlargement remains obscure. While it is difficult absolutely to exclude an unusual and exaggerated response to an exogenous infection or infections, there was no evidence for this. An alternative possibility is that some at least of the patients were suffering from a type of auto-immune disease, the main feature being exaggerated lympho-reticular cellular proliferation, particularly within the spleen, rather than antibody formation. In some patients the lymphoproliferation was so marked as to suggest the development of a chronic ‘pre-malignant’ lymphoma, predominantly (but not exclusively) affecting the spleen.     

乙型肝炎肝硬化患者中医证型与超声影像学特征的关系

目的:探讨乙型肝炎肝硬化患者中医证型与肝脾大小及门静脉血流动力学的关系。方法:用彩超仪检测150例不同中医证型肝硬化(分为6型)患者的肝右叶最大斜径、前后径,肝左叶上下径、前后径,门静脉及脾静脉内径、血流速度,脾脏大小等超声指标,进行对比分析。结果:肝硬化血瘀证患者与肝气郁结证、湿热内蕴证、肝肾阴虚证患者相比,肝左叶上下径的差异有显著性意义(P<0.05);肝硬化湿热内蕴证患者与血瘀证患者相比,脾脏厚度差异有显著性意义(P<0.05);肝硬化湿热内蕴证患者与肝肾阴虚证、脾肾阳虚证、血瘀证患者相比,门静脉主干内径差异有显著性意义(P<0.05);肝硬化血瘀证患者与肝气郁结证患者相比,门静脉血流流速差异有显著性意义(P<0.01);脾静脉内径、血流流速各型之间比较差异无显著性意义。结论:超声检查对肝硬化中医辨证分型有一定指导意义,随着证型的发展,肝脾大小及门静脉血流动力学有相应改变。     

The development and clinical features of splenic aneurysm associated with liver cirrhosis.

OBJECTIVES: Splenic artery aneurysm (SAA) is usually asymptomatic, but can be fatal if it ruptures. Portal hypertensive patients with varix or splenomegaly are sometimes complicated by SAA. However, there have been no large-scale clinical studies regarding whether liver cirrhosis itself is associated with splenic aneurysm regardless of varix or splenomegaly. METHODS: In the present study, we retrospectively analyzed 303 cirrhotic patients examined with arteriography. The diagnosis and characteristics of SAAs were determined, and the relation with splenic artery diameter was evaluated. RESULTS: Nine patients (2.97%) had 12 complicated SAAs. The aneurysms, which measured 4-22 mm in diameter, were all saccular, and occurred commonly in the splenic hilum (50.0%). A correlation was noted between splenic artery diameter and aneurysm diameter (R(2)=0.706). Aneurysm growth was strongly associated with an increase in diameter of the splenic artery trunk (R(2)=0.705), which is closely related to arterial flow. CONCLUSIONS: SAA is considered a complication of cirrhosis. The increase in splenic artery diameter may result in SAA enlargement and rupture. Elective procedures should be considered based on the follow-up of main trunk or diameter of the splenic artery in addition to SAA size, a known risk factor of aneurysmal rupture.     

Change in portal flow after liver transplantation: effect on hepatic arterial resistance indices and role of spleen size

Information on changes in splanchnic hemodynamics after liver transplantation is incomplete. In particular, data on long-term changes are lacking, and the relationship between changes in arterial and portal parameters is still under debate. The effect of liver transplantation on splanchnic hemodynamics was analyzed with echo-Doppler in 41 patients with cirrhosis who were followed for up to 4 years. Doppler parameters were also evaluated in 7 patients transplanted for acute liver failure and in 35 controls. In cirrhotics, portal blood velocity and flow increased immediately after transplantation (from 9.1 plus minus 3.7 cm/sec to 38.3 plus minus 14.6 and from 808 plus minus 479 mL/min to 2,817 plus minus 1,153, respectively, P <.001). Hepatic arterial resistance index (pulsatility index) also augmented (from 1.36 plus minus 0.32 to 2.34 plus minus 1.29, P <.001) and was correlated with portal blood velocity and flow. The early changes in these parameters were related, in agreement with the hepatic buffer response theory. Portal flow returned to normal values after 2 years. Superior mesenteric artery flow normalized after 3 to 6 months. Splenomegaly persisted after 4 years, when spleen size was related to portal blood flow. In 7 patients transplanted for acute liver failure, portal flow, and hepatic arterial resistance index were normal after transplantation. In conclusion, a high portal flow was present in cirrhotics until 2 years after transplantation, probably because of maintenance of elevated splenic flow. An early increase in hepatic arterial resistance indices is a common finding, but it is transient and is related to the increase in portal blood flow. A normal time course of portal-hepatic hemodynamics was detected in patients transplanted for acute liver failure.     

Hypersplenism induced by hepatectomy

BACKGROUND/AIMS: We encountered a case of posthepatectomy splenic enlargement and hypersplenism followed by disseminated intravascular coagulopathy with airway hemorrhage causing death. METHODOLOGY: We, therefore, retrospectively investigated postoperative splenic enlargement, hypersplenism and disseminated intravascular coagulopathy by computed tomography and laboratory data in 57 hepatectomized patients with a malignant or benign disease in the postoperative period. RESULTS: Of 32 patients with hepatocellular carcinoma or biliary tract carcinoma (group A), 12 with metastatic hepatic lesions (group B), and 13 with benign liver disease (group C); remarkable (20%) splenic enlargement was noted in 8 patients in group A, 2 in group B, and 2 in group C. Seven of the 12 patients were associated with liver cirrhosis, 5 with preoperative splenomegaly, and 8 had undergone major hepatectomy. Postoperative hypersplenism developed in 5 patients in group A, and one patient in group C. All of them were associated with liver cirrhosis or chronic hepatitis and preoperative splenomegaly, and five had undergone hepatic lobectomy or more extensive resections. All except for the disseminated intravascular coagulopathy case recovered. Statistically, splenic enlargement was significantly related to the extent of hepatectomy; lobectomy versus segmentectomy = 28.3 +/- 28.5% (n = 14) versus 12.4 +/- 13.8% (n = 20), (unpaired Student's t test, P = 0.037). Platelet counts of the patients with liver cirrhosis or chronic hepatitis is lower than those without the diseases, both pre- and postoperatively (14.0 +/- 6.0 x 10(4)/mm3 vs. 21.5 +/- 6.2 x 10(4)/mm3, P = 0.0001). CONCLUSIONS: Postoperative hypersplenism was noted only in the patients with liver cirrhosis or chronic hepatitis and preoperative splenomegaly, and developed more frequently after larger hepatectomies than after smaller hepatectomies; 5 (45%) of 11 versus 1 (7%) of 14, chi 2 test, P = 0.026).     

Platelet dynamics in chronic liver disease using the 111Indium oxine label

Platelet dynamics in chronic liver disease have been studied using 111Indium-8-hydroxyquinolone (111In-oxine) as a platelet label. In 20 patients, mainly with alcoholic cirrhosis, the platelet mean life span was reduced in 12 and the splenic platelet pool increased, often markedly so, in 15. However, the platelet count was not significantly related to mean bile span, the splenic platelet pool, or spleen size. Whereas splenic platelet pool size is related to spleen size in most of the haematological 'big-spleen' syndromes, this did not apply to those patients with chronic liver disease. Technically, 111In-oxine is a more appropriate platelet label than 51Cr in ill and thrombocytopenic patients with liver disease.