Should Portosystemic Shunt Be Reconsidered in the Treatment of Intractable Ascites in Cirrhosis?

Franco, Dominique; Vons, C.; Traynor, O.; Smadja, Claude

doi:10.1001/archsurg.1988.01400320073015

Cited by 72 publications

(46 citation statements)

References 25 publications

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“…14 When the heart is stimulated by b-adrenergic agonists, the such a notion. However, a direct acute toxic effect on cell membranes seems unlikely given that the studies were percontractile responses are expected to increase both inotropically (the contractile force) and chronotropically (the heart formed at least 1 week after the last dose of CCl 4 .…”

Section: Impaired Contractility Undermentioning

confidence: 99%

Cirrhotic cardiomyopathy: Getting to the heart of the matter

1996

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can lead to liver dysfunction and damage. How unexpected In cirrhosis, cardiac contractile function has been exand gratifying, therefore, to find a voice as eloquent as the tensively documented to be abnormal. At baseline, carlate Chilean Nobel laureate's to not only extoll the many diac output is increased, and this is one of the charactervirtues of the liver, but also remind us that sometimes the istics of hyperdynamic circulation. However, when liver takes precedence over the heart, i.e., that liver failure cirrhotic patients are challenged by pharmacological or can also lead to cardiac dysfunction. physiological stress, ventricular hyporesponsiveness is It has been known for more than four decades that hepatic revealed. Similar patterns have been noted in cirrhotic cirrhosis is associated with a host of cardiovascular abnoranimal models. This phenomenon has been termed ''cirmalities. The initial studies in the early 1950s documented rhotic cardiomyopathy.'' Although alcohol abuse may the existence of hyperdynamic circulation in cirrhosis, manicontribute to some cases of cirrhotic cardiomyopathy, it has been clearly documented to occur even in the ab-fested by increased cardiac output and reduced systemic vassence of alcohol ingestion. Diminished myocardial b-ad-cular resistance. This latter phenomenon, the peripheral varenergic receptor signal transduction function, possibly sodilatation, continues to fascinate investigators even up to caused by a persistent elevation in norepinephrine con-the present, and recent studies have examined the possible tent, has been shown to play an important role. Alter-role of nitric oxide and other endothelium-dependent factors ation in cardiac plasma membrane properties due to im-in mediating the vasodilatation. The heart itself was not expaired lipid metabolism is also crucial. Other possible amined until about three decades ago, and around that time pathogenic factors are reviewed, including accumula-studies of cardiac contractile function in patients with alcotion of cardiodepressant substances caused by hepato-holic-induced liver disease started consistently showing that cellular insufficiency, and ventricular overload sec-despite the increased baseline cardiac output, when ventricuondary to increased blood volume and hyperdynamic lar contractile responses were tested under conditions of circulation. Because the cardiac reserve function is bor-pharmacological or physiological stress, the heart behaved derline in patients with cirrhosis, cardiovascular status abnormally in a blunted manner. For many years, this was should be carefully monitored, especially when patients ascribed to the well-known direct toxic effects of alcohol on undergo stresses such as liver transplantation or porto-cardiac muscle, i.e., as a manifestation of latent or subclinical systemic shunting procedures. (HEPATOLOGY 1996;24: alcoholic cardiomyopathy, and relegated to the scientific 451-459.)backwaters as a clinically insignificant curiosity. However, recently several studies have emerged in both ...

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Section: Impaired Contractility Undermentioning

confidence: 99%

Cirrhotic cardiomyopathy: Getting to the heart of the matter

1996

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“…Cirrhotic patients were noted to have resting tachycardia, warm peripheries, a bounding pulse, and a wide pulse pressure, but these findings were attributed to the effects of alcohol on the circulation. Beginning in the late 1980s, occasional reports of unexpected deaths due to heart failure following liver transplantation [2], transjugular intrahepatic portosystemic stent shunt (TIPS) insertion [3], and surgical portocaval shunts [4] led to an upsurge of interest in investigating for cardiac dysfunction related to cirrhosis. There followed detailed studies assessing the cardiovascular complications of cirrhosis.…”

Section: Introductionmentioning

confidence: 99%

Cirrhotic cardiomyopathy

2008

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Cirrhotic cardiomyopathy is a recently recognized condition in cirrhosis consisting of systolic incompetence under condition of stress, diastolic dysfunction related to altered diastolic relaxation, and electrophysiological abnormalities in the absence of any known cardiac disease. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers such as brain natriuretic factor. The underlying pathogenetic mechanisms include abnormalities in the b-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects. Various compounds for which levels are elevated in cirrhosis such as nitric oxide and carbon monoxide can also exert a negative inotropic effect on the myocardium, whereas excess sodium and volume retention can lead to myocardial hypertrophy. Various toxins can also aggravate the ion channel defects, thereby widening the QRS complex causing prolonged QT intervals. Clinically, systolic incompetence is most evident when cirrhotic patients are placed under stress, whether physical or pharmacological, or when the extent of peripheral arterial vasodilatation demands an increased cardiac output as in the case of bacterial infections. Acute volume overload such as immediately after insertion of a transjugular intrahepatic portosystemic shunt or after liver transplantation can also tip these cirrhotic patients into cardiac failure. Treatment of cirrhotic cardiomyopathy is unsatisfactory. There is some evidence that b-blockade may help some cirrhotic patients with baseline prolonged QT interval. Long-term aldosterone antagonism may help reduce myocardial hypertrophy. Future studies should include further elucidation of pathogenetic mechanisms so as to develop effective treatment strategies.

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“…In other words, RA may not be mobilized or early reappearance after treatment and may not be prevented by medical therapies. Several different therapeutic approaches have been tested in cirrhotic patients with RA; including, surgical portocaval anastomosis [11], paracentesis with i.v. albumin infusion [12], transjugular intrahepatic portacaval shunt [12] and diuretics [13].…”

Section: Discussionmentioning

confidence: 99%

High Dose Oral Furosemide with Salt Ingestion in the Treatment of Refractory Ascites of Liver Cirrhosis

Yakar¹,

Demır²,

Doğan³

et al. 2016

CIM

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Purpose: We aimed to evaluate and compare the efficacy and safety of high-dose furosemide+salt orally by comparing HSS+ furosemide (i.v.) and repeated paracentesis in patients with RA.Methods: This was a prospective study of 78 cirrhotic patients with RA, randomized into three groups: Group A (n= 25) i.v. furosemide (200-300 mg bid) and 3% hypotonic saline solution (HSS) (once or twice a day); Group B (n= 26) oral furosemide tablets (360-520 mg bid) and salt (2.5 g bid); and, Group C (n= 27) repeated large-volume-paracentesis (RLVP) with albumin infusion. Patients without hyperkalemia were administrated 100 mg of spironolactone/day. During the follow-up; INR, creatinine, and total bilirubin levels were measured to determine the change in MELD (model of end stage liver disease) score.Results: Hepatic encephalopathy (HE), severe episodes of spontaneous bacterial peritonitis (SBP) and pleural effusions (PE) occurred more frequently in Group C. Improvement in Child-Pugh and MELD score was better in Group A and B than Group C. In Group B, improvements were seen in the Child-Pugh and MELD score, reduction in body weight, duration and number of hospitalization. In Groups A and B, remarkable increases in diuresis were observed (706±116 to 2425±633 mL and 691±111 to 2405±772 mL) and serum sodium levels also improved. HE and SBP were occurred more often in group C (p<0.002). Hospitalization decreased significantly in Group B (p<0.001). There was no significant difference in survival among groups. Conclusion:High dose oral furosemide with salt ingestion may be an alternative, effective, safe and well-tolerated method of therapy for RA.SUPPLEMENT

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Should Portosystemic Shunt Be Reconsidered in the Treatment of Intractable Ascites in Cirrhosis?

Cited by 72 publications

References 25 publications

Cirrhotic cardiomyopathy: Getting to the heart of the matter

Cirrhotic cardiomyopathy: Getting to the heart of the matter

Cirrhotic cardiomyopathy

High Dose Oral Furosemide with Salt Ingestion in the Treatment of Refractory Ascites of Liver Cirrhosis

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