Haemodynamic adaptation two months after transjugular intrahepatic portosystemic shunt (TIPS) in cirrhotic patients.

BACKGROUND AND AIMS: In portal hypertensive patients, transjugular intrahepatic portosystemic shunt (TIPS) acutely increases cardiac output and exaggerates peripheral vasodilatation. It has been suggested that the worsened hyperdynamic state may progress to high output heart failure. The aim was to evaluate the acute and short-term haemodynamic adaptation to this procedure. METHODS: Systemic, splanchnic, and pulmonary haemodynamics were studied in 15 cirrhotic patients under stable haemodynamic conditions before placement of TIPS, then 15-30 minutes after and two months later. For inclusion in the final analysis, an uneventful post-TIPS at two months follow up and a stable portacaval gradient were required. The following variables were measured or calculated: portacaval gradient; cardiac index (thermodilution); systolic and diastolic mean arterial, atrial, pulmonary arterial, and wedged pulmonary capillary pressures; heart rate; and total peripheral and pulmonary vascular resistances. Blood flow in the shunt was measured using duplex Doppler ultrasound. RESULTS: The portacaval gradient decreased by 56% and remained stable thereafter. Shunt blood flow was unchanged when measured immediately after TIPS and two months later. Immediately after TIPS there was a pronounced increase in cardiac index (+32%; p < 0.05) in association with a decrease in peripheral and pulmonary vascular resistance (-21%; p < 0.05 and -14%; NS). Two months later, whereas the initial rise in cardiac index was attenuated, peripheral vascular resistances remained similar and pulmonary vascular resistances decreased further (-33%; p < 0.05) compared with immediate post-TIPS values. CONCLUSIONS: Hyperdynamic circulation worsened immediately after TIPS, with a progressive adaptation during follow up. The mechanisms of post-TIPS induced haemodynamic changes include an abrupt volume load resulting from splanchnic decompression and an increased delivery of gut derived vasodilators to the systemic circulation. The persistence of decreased peripheral and pulmonary vascular resistances despite the reduction in high cardiac output two months after TIPS suggests that vasodilatation is not solely a compensatory response to a TIPS induced increased preload. Vasodilatory substances shunted away from the liver probably play an important part in this phenomenon.

Analisis de pacientes con pancreatitis aguda (PA), decada (1984-1994) comparacion con serie anterior / Analysis of patients with acute pancreatitis (AP), (1984-1994) comparation with serie anterior

Se revisaron las historias clínicas de 190 pacientes internados entre 1984 y 1994 con diagnóstico de pancreatitis aguda. Tuvieron confirmación quirúrgica 141, necrópsica 1 (75 por ciento), y las restantes confirmadas por la evolución clínica y TAC. El sexo femenino 122 (64 por ciento), masculino 68 (36 por ciento), media de edad de 41 años (mínima 7, máxima 82). La etiología fue biliar en 129 (68 por ciento) con 4 fallecidos (3 por ciento), alcohólica en 26 (14 por ciento), con 5 fallecidos (19 por ciento), idiopática en 24 (13 por ciento) y miscelánea 11 (5 por ciento), las dos últimos sin mortalidad. La mortalidad global fue del 5 por ciento (9/190). Se efectuó tratamiento quirúrgico en 141 (74 por ciento) y endoscópico en 2 (1 por ciento), 47 pacientes (25 por ciento) no fueron operados. El grupo PA leve estuvo conformado por 154 pacientes (81 por ciento) con un score de Tanson promedio de 2.2 y sin mortalidad. Se indicó cirugía de urgencia en 7 (6 por ciento), temprana en 3 (3 por ciento), tardía en 1 (0,9 por ciento) u programada en 99 (90 por ciento). En el grupo de PA grave hubo 36 pacientes (19 por ciento) con un score promedio de Ranson de 4.2. Fallecieron 9 (25 por ciento). Se operaron 31 pacientes, de estos 17 (47 por ciento) de urgencia, 1 (3 por ciento) cirurgía temprana y 13 (36 por ciento) tardía. Se compararon las cifras de mortalidad de este grupo, con otra serie del mismo Hospital entre 1975-1984. Comparando los dos series se observó en el grupo 1984-1994: disminución significativa de la mortalidad global 4.7 por ciento vs 12.7 por ciento (p=0.0047); en la mortalidad de la etiologia biliar 3.1 por ciento vs 11.2 por ciento (p=0.0087); sin mortalidad en las etiologías idiopáticas y miscelánea, comparada 18.7 por ciento y 20 por ciento respectivamente de la serie anterior; mortalidad nula de la PA leve comparada con el 5 por ciento de la serie anterior y por último de la PA leve comparada con el 5 por ciento de la serie anterior y por último la mortalidad en la forma grave fue menor 25 por ciento vs 40.8 por ciento. Consideramos como causa de este avance mejor diagnóstico, evaluación temprana de la severidad, medidas de apoyo sistémico en las formas graves, la administración de antibióticos de mayor espectro y penetración en el páncreas y especialmente el cambio en el tiempo de indicación quirúrgica. Mientras que en el primer período se optó por la cirurgía temprana sobre el páncreas, en el segundo se indicó intervención diferida, salvo en casos especiales.

Analisis de pacientes con pancreatitis aguda (PA), decada (1984-1994) comparacion con serie anterior / Analysis of patients with acute pancreatitis (AP), (1984-1994) comparation with serie anterior

Se revisaron las historias clínicas de 190 pacientes internados entre 1984 y 1994 con diagnóstico de pancreatitis aguda. Tuvieron confirmación quirúrgica 141, necrópsica 1 (75 por ciento), y las restantes confirmadas por la evolución clínica y TAC. El sexo femenino 122 (64 por ciento), masculino 68 (36 por ciento), media de edad de 41 años (mínima 7, máxima 82). La etiología fue biliar en 129 (68 por ciento) con 4 fallecidos (3 por ciento), alcohólica en 26 (14 por ciento), con 5 fallecidos (19 por ciento), idiopática en 24 (13 por ciento) y miscelánea 11 (5 por ciento), las dos últimos sin mortalidad. La mortalidad global fue del 5 por ciento (9/190). Se efectuó tratamiento quirúrgico en 141 (74 por ciento) y endoscópico en 2 (1 por ciento), 47 pacientes (25 por ciento) no fueron operados. El grupo PA leve estuvo conformado por 154 pacientes (81 por ciento) con un score de Tanson promedio de 2.2 y sin mortalidad. Se indicó cirugía de urgencia en 7 (6 por ciento), temprana en 3 (3 por ciento), tardía en 1 (0,9 por ciento) u programada en 99 (90 por ciento). En el grupo de PA grave hubo 36 pacientes (19 por ciento) con un score promedio de Ranson de 4.2. Fallecieron 9 (25 por ciento). Se operaron 31 pacientes, de estos 17 (47 por ciento) de urgencia, 1 (3 por ciento) cirurgía temprana y 13 (36 por ciento) tardía. Se compararon las cifras de mortalidad de este grupo, con otra serie del mismo Hospital entre 1975-1984. Comparando los dos series se observó en el grupo 1984-1994: disminución significativa de la mortalidad global 4.7 por ciento vs 12.7 por ciento (p=0.0047); en la mortalidad de la etiologia biliar 3.1 por ciento vs 11.2 por ciento (p=0.0087); sin mortalidad en las etiologías idiopáticas y miscelánea, comparada 18.7 por ciento y 20 por ciento respectivamente de la serie anterior; mortalidad nula de la PA leve comparada con el 5 por ciento de la serie anterior y por último de la PA leve comparada con el 5 por ciento de la serie anterior y por último la mortalidad en la forma grave fue menor 25 por ciento vs 40.8 por ciento. Consideramos como causa de este avance mejor diagnóstico, evaluación temprana de la severidad, medidas de apoyo sistémico en las formas graves, la administración de antibióticos de mayor espectro y penetración en el páncreas y especialmente el cambio en el tiempo de indicación quirúrgica. Mientras que en el primer período se optó por la cirurgía temprana sobre el páncreas, en el segundo se indicó intervención diferida, salvo en casos especiales. (AU)

The role of central blood volume in the development of sodium retention in portal hypertensive rats.

BACKGROUND & AIMS: In portal hypertension, peripheral vasodilatation (PVD) causes Na+ retention as a result of vascular underfilling. The central blood volume is responsible for the vascular filling signals to baroreceptors and volume receptors. The aim of this study was to determine the role of central blood volume in Na+ retention in portal hypertensive rats. METHODS: Mean arterial pressure, portal pressure, cardiac output, total peripheral resistance, central blood volume, and extracellular Na+ space were assessed daily in rats after portal vein ligation or sham operation until a hyperdynamic circulatory state developed. RESULTS: On day 1, portal vein-ligated rats had PVD and a diminished central blood volume (1.26 +/- 0.04 vs. 1.47 +/- 0.09 mL/100 g body wt; P < 0.05). On day 2, Na+ space increased in portal vein-ligated rats (38.1 +/- 0.5 vs. 33.1 +/- 0.5 mL/100 g body wt; P < 0.01). From day 2 on, normalization of central blood volume and cessation of Na+ retention were observed despite persistent PVD. On day 4, portal vein-ligated rats developed a hyperdynamic circulatory state with a normal central blood volume and persistent PVD. CONCLUSIONS: Although total peripheral resistance remains decreased, Na+ retention ceases after central blood volume is normalized. Central blood volume therefore appears to be the signal for Na+ retention. Although PVD persists after Na+ retention ceases, it may contribute to Na+ retention by decreasing central blood volume.

[Analysis of patients with acute pancreatitis (AP), (1984-1994) decade. Comparison with a past series]. / Análisis de pacientes con pancreatitis aguda (PA), Década (1984-1994). Comparación con serie anterior.

Between 1984-1994 records of 190 patients with acute pancreatitis (AP) were reviewed. Diagnosis was confirmed by surgery in 141, by necropsy 1 (75%), and for the remaining patients, by CT and clinical evaluation. Female 122 were female (64%), male 68 (36%), mean age 41 years (range 7-82 years). The etiologic factors were gallstones in 129 (68%) with 4 deaths (3%), alcoholic in 26 (14%) with 5 (19%) deaths, idiopathic in 24 (13%) and miscellaneous 11 (5%), the last 2 without mortality. The overall mortality was 5% (9/190). Surgical treatment was indicated in 141 (74%) and endoscopic treatment in 2 (1%), 47 patients (25%) received only medical treatment. One-hundred and fifty-four patients (81%) were mild forms with a Ranson mean score 2.2 without mortality. In this group, emergency surgery was indicated in 7 (6%), early in 3 (3%), late in 1 (0.9%) and elective in 99 (90%). In the severe group were 36 patients (19%) with a mean Ranson score of 4.2. Nine patients died (25%), 31 were surgically treated, by emergency surgery in 17 (47%), 1 (3%) early surgery and 13 (36%) late surgery. The mortality rate of this group was compared with previous series of the same hospital (1975-1984 series). The 1984-1994 group showed a significant overall mortality decrease 4.7% vs 12.7% (p = 0.0047); 3.1% vs 11.2% (p = 0.0087) for the gallstones group; without mortality in the idiopathic and miscellaneous form compared with 18.7% and 20% respectively of the previous series; no mortality was observed in the mild AP compared with 5% of the previous series. The mortality in the severe form was 25% vs 40.8% (1975-1984 group). We consider that the decreased mortality could be attributed to the improvement in the diagnosis, early recognition of the severe forms, systemic supportive care in the severe forms, the use of antibiotics with wide spectrum and deeper penetration in the pancreas and specially in the change of the surgical timing. Although, in the first period the option was the early pancreatic surgery, in the second this was indicated only in particular cases.

Short- and long-term hemodynamic effects of transjugular intrahepatic portosystemic shunts: a Doppler/manometric correlative study.

OBJECTIVE: The purposes of this study were to evaluate the effect of a well-functioning transjugular intrahepatic portosystemic shunt (TIPS) on the splanchnic and intrahepatic circulation, to determine if sonographic measurements can predict shunt dysfunction before clinical manifestations of portal hypertension occur, and to compare Doppler sonographic findings with portocaval gradient measurements before and after shunt revision. SUBJECTS AND METHODS: Forty-four patients with cirrhosis (n = 43) and myelofibrosis (n = 1) who underwent successful TIPS insertion were included in this prospective study. Indications for TIPS placement were: refractory ascites (24 patients), bleeding esophageal varices (17 patients), portal hypertensive gastropathy (two patients), and bleeding colonic varices (one patient). The portal vein and the inferior vena cava were catheterized; and the portocaval gradient was recorded before TIPS placement, at 2 and 12 months after TIPS placement, and when clinical or Doppler findings suggested shunt dysfunction. Doppler studies were done within 1 week before TIPS placement, within 2 days after TIPS placement, every 2-3 months thereafter, and before and after a TIPS revision. The Doppler studies included flow volume measurements in the portal vein and in the stent, as well as determination of the direction of flow in the segmental branches of the portal vein, in the splanchnic veins, and in portosystemic collaterals. Changes in Doppler findings and in catheter pressure measurements were compared using Spearman's rank correlation test. Significance was set at the .05 level. RESULTS: A marked decrease (-51%) in portocaval gradient was observed after TIPS placement. At Doppler sonography, portal vein velocity and diameter were both higher after TIPS placement, resulting in a marked increase in portal venous flow (170%). Mean flow velocity in the shunt was 55.8 +/- 3.6 cm/sec, and flow volumes in the shunt and in the main portal vein were 1596 ml/min and 1731 ml/min, respectively (p = nonsignificant). Dysfunction of the stent occurred in 27% of the patients. Changes in stent blood flow volume were closely related to changes in the portocaval gradient (r = -0.67, p < .001). Reduction of blood flow volume in the stent or change of direction of flow in intrahepatic portal veins or in collateral veins signaled shunt dysfunction (84% sensitivity, 89% specificity). CONCLUSION: Marked hemodynamic changes in the portal venous system occur soon after a TIPS procedure. Monitoring of shunt function with periodic Doppler sonography, including calculation of shunt blood flow, is useful in detecting shunt dysfunction before clinical signs occur.

Autoimmune cholangiopathy: the result of consecutive primary biliary cirrhosis and autoimmune hepatitis?

Autoimmune cholangiopathy is a recently proposed entity that describes a specific group of patients presenting overlapping features of primary biliary cirrhosis and autoimmune hepatitis, i.e., clinical and/or biochemical cholestasis, high titer antinuclear antibody, negative antimitochondrial antibody, and elevated immunoglobulin G. Liver histology shows primary biliary cirrhosis coexisting with varying degrees of parenchymal inflammation. In addition, these patients achieve remission on corticosteroid therapy. The patient in this report fulfilled the above criteria. However, preceding the autoimmune cholangitis stage, a typical antimitochondrial antibody-positive primary biliary cirrhosis was documented with favorable response to ursodeoxycholic acid treatment. Twenty months later, the patient developed autoimmune hepatitis with elevated aspartate aminotransferase and immunoglobulin G and high titer antinuclear antibody as well as corticosteroid dependency, whereas the antimitochondrial antibody disappeared. The patient's sera initially showed reactivity to three mitochondrial proteins, the 74-, 64-, and 56-kilodalton autoantigens of the 2-oxo acid dehydrogenase complexes, which was characteristic of primary biliary cirrhosis. After developing autoimmune hepatitis, reactivity to the 74- and 64-kilodalton antigens disappeared, whereas reactivity to the 56-kilodalton antigen decreased to low levels. Autoimmune cholangitis and probably other forms of the overlap syndrome may result from the association of two diseases: primary biliary cirrhosis and autoimmune hepatitis.

Administration of N omega-nitro-L-arginine ameliorates portal-systemic shunting in portal-hypertensive rats.

BACKGROUND: Nitric oxide, a vasodilator synthesized from L-arginine by vascular endothelial cells, may play a role in the development of portal-systemic collaterals. This study investigated the effect of long-term inhibition of NO secretion on portal systemic shunting. METHODS: Systemic and splanchnic hemodynamics and the degree of portal-systemic shunting were evaluated in partial portal vein-ligated rats after administration of placebo (0.9% saline) or N omega-nitro-L-arginine (NNA) (approximately 2 micrograms.kg-1 x min-1) intravenously for 6 days. RESULTS: NNA treatment induced increases in splanchnic arterial resistance (P < 0.001) and portal-collateral resistance (P < 0.05) and a decrease in portal venous inflow (P < 0.05). Portal pressure was not changed (NS). The splenic-systemic shunting was significantly decreased from 81% +/- 5% in the placebo-treated group to 69% +/- 4% in the NNA-treated group (P < 0.05), paralleled by an insignificant reduction in the mesenteric-systemic shunting (64% +/- 7% vs. 50% +/- 6%, NS). The attenuation of portal-systemic shunting by NNA was further shown by an increase in the vascular resistance of portal-systemic collateral venous bed using an in situ portal-systemic collateral perfusion model (1.27 +/- 0.05 vs. 1.07 +/- 0.03 cm H2O.mL-1 x min-1; P < 0.001). CONCLUSIONS: The results show that in portal hypertensive rats, NNA reduces portal-systemic shunting without reducing portal pressure, suggesting that NO plays a role in the collateralization of the portal system. In addition, high flow through the portal-collateral bed is probably an important driving force that is independent of portal hypertension for the development of portal-systemic shunting in portal-hypertensive rats.

Octreotide ameliorates vasodilatation and Na+ retention in portal hypertensive rats.

BACKGROUND: Whether long-term octreotide treatment given to portal hypertensive rats could prevent or ameliorate peripheral vasodilatation and thereby modify sodium retention was investigated. METHODS: Starting at the time of partial portal vein ligation or sham operation, rats received a 4-day course of either octreotide (15 micrograms/kg in 5% dextrose in water) or placebo (5% dextrose in water) subcutaneously every 8 hours. RESULTS: In portal hypertensive rats, octreotide induced a 13% increase in mean arterial pressure (P < 0.01) and a 19% increase in total peripheral resistance (P < 0.01). Octreotide treatment induced a decrease in extracellular sodium space (22Na injection) (34.2 +/- 0.5 vs. 36.7 +/- 0.4 mL/100 g; P < 0.01) without changes in serum sodium level. In addition, octreotide treatment significantly reduced portal pressure as well as glucagon levels and plasma renin activity. In contrast, octreotide treatment had no effect on mean arterial pressure and extracellular sodium space in shamoperated rats. CONCLUSIONS: Long-term octreotide treatment ameliorated peripheral vasodilatation and sodium retention only in portal hypertensive rats. These findings suggest that in portal hypertension sodium retention can be modified by pharmacological agents that affect peripheral vasodilatation. The specificity of octreotide's effect sheds additional light into the vasodilatory syndrome associated with portal hypertension in liver diseases.

N omega-nitro-L-arginine administration corrects peripheral vasodilation and systemic capillary hypotension and ameliorates plasma volume expansion and sodium retention in portal hypertensive rats.

In portal hypertensive states, peripheral vasodilation leads to sodium retention and plasma volume expansion. N omega-nitro-L-arginine, a specific biosynthesis inhibitor of the vasodilator nitric oxide, has been shown to acutely reverse peripheral vasodilation and the vascular hyporesponsiveness to endogenous and exogenous vasoconstrictors observed in portal hypertensive rats. This study investigated whether N omega-nitro-L-arginine treatment in portal hypertensive rats prevents peripheral vasodilation and therefore ameliorates plasma volume expansion and sodium retention. For 2 days before partial portal vein ligation or sham operation and then continuously for 4 days after the operation, animals received either placebo (0.9% saline) or N omega-nitro-L-arginine (approximately 2 micrograms/kg/min) intravenously through a subcutaneously implanted Alzet osmotic pump (model 2ML1; Alza, Palo Alto, CA). In portal hypertensive rats, N omega-nitro-L-arginine treatment significantly increased mean arterial pressure (placebo vs. N omega-nitro-L-arginine, 123 +/- 4 vs. 150 +/- 2 mm Hg, respectively; p < 0.001) and systemic vascular resistance (3.8 +/- 0.2 vs. 5.6 +/- 0.3 mm Hg/ml/min/100 gm body weight; p < 0.001), associated with a decrease in the cardiac index (33.5 +/- 1.0 vs. 27.0 +/- 1.1 ml/min/100 gm body weight; p < 0.001). N omega-nitro-L-arginine treatment also induced a decrease in plasma volume (4.6 +/- 0.1 vs. 4.1 +/- 0.1 ml/100 gm body weight; p < 0.001) and extracellular sodium space (39.4 +/- 0.7 vs. 37.4 +/- 0.4 ml/100 gm body weight; p < 0.05) without changes in serum sodium.(ABSTRACT TRUNCATED AT 250 WORDS)