Brachial and femoral artery blood flow in cirrhosis: Relationship to kidney dysfunction

Maroto, Albert; Ginès, Pere; Arroyo, Vicente; Ginés, Àngels; Saló, Joan; Clària, Joan; Jiménez, Wladimiro; Brú, Concepció; Rivera, Francisca; Rodés, Joan

doi:10.1002/hep.1840170507

Cited by 71 publications

(103 citation statements)

References 31 publications

(19 reference statements)

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“…Contrasting data from the literature show that in cirrhotic patients muscular perfusion can be increased or normal [20,21]. Recent studies have reported that brachial and/or femoral artery blood flow investigated with Doppler techniques is normal, as is capillary skin blood flow studied by nuclear medicine techniques [22].…”

Section: Cutaneus and Muscular Manifestationsmentioning

confidence: 91%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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Section: Cutaneus and Muscular Manifestationsmentioning

confidence: 91%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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“…9 Therefore, in decompensated cirrhosis there is vasoconstriction in all major vascular territories except in the splanchnic circulation, in which there is a generalized arteriolar vasodilation. Splanchnic arteriolar vasodilation is, therefore, the initial event of circulatory dysfunction in cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

“…9 It has been proposed that the increased resistance in these vascular territories is a homeostatic response which is mediated by the sympathetic nervous system, renin-angiotensin system, and other vasoconstrictors to counteract the deleterious effect of the splanchnic arteriolar vasodilation on the systemic circulation and, therefore, to maintain arterial pressure. 8,9 During the last years, considerable interest has been focused on the cerebral circulation in acute and chronic liver disease. Using transcranial Doppler ultrasonography in the middle cerebral artery, Larsen et al 10 and Lagi et al 11 have recently reported that cerebral autoregulation is impaired in some patients with cirrhosis.…”

mentioning

confidence: 99%

“…Interestingly enough, renal perfusion in cirrhotic patients correlates directly with brachial and femoral blood flow; both measurements correlate inversely with the plasma levels of renin. 9 It has been proposed that the increased resistance in these vascular territories is a homeostatic response which is mediated by the sympathetic nervous system, renin-angiotensin system, and other vasoconstrictors to counteract the deleterious effect of the splanchnic arteriolar vasodilation on the systemic circulation and, therefore, to maintain arterial pressure. 8,9 During the last years, considerable interest has been focused on the cerebral circulation in acute and chronic liver disease.…”

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confidence: 99%

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Increased cerebrovascular resistance in cirrhotic patients with ascites

et al. 1998

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Studies assessing regional hemodynamics in patients with cirrhosis and ascites have shown vasodilation in the splanchnic circulation and vasoconstriction in the renal circulation and in the brachial and femoral artery vascular territories. The aim of this study was to assess the cerebral vascular resistance in cirrhotic patients with ascites. The resistive index in the middle cerebral artery (an index of the cerebral vascular resistance) and in a renal interlobar artery were measured by Doppler ultrasonography in 7 healthy subjects: 13 patients with compensated cirrhosis and 24 patients with ascites (13 with renal failure). The arterial blood pressure and the activity of the renin-angiotensin and sympathetic nervous systems, as estimated by plasma renin activity and plasma norepinephrine concentration, respectively, were also measured. The resistive index in the middle cerebral artery was significantly increased in patients with ascites (0.68 ؎ 0.05, mean ؎ SD) as compared with patients without ascites (0.60 ؎ 0.01, P F .05) and with healthy patients (0.52 ؎ 0.01, P F .01). Renal resistive index was also increased in patients with ascites (0.77 ؎ 0.01) compared with the other two groups (0.68 ؎ 0.02 and 0.62 ؎ 0.00, respectively; P F .001). The resistive index in the middle cerebral artery showed a direct correlation with renal resistive index (r ‫؍‬ .73, P F .01), plasma renin activity (r ‫؍‬ .61, P F .01), and norepinephrine (r ‫؍‬ .53, P F .01). The resistive index in the middle cerebral artery showed an inverse correlation with mean arterial pressure (r ‫,54.؊؍‬ P F .01). These results indicate that in patients with cirrhosis and ascites there is a cerebral vasoconstriction which is probably related with the arterial hypotension and the overactivity of vasoconstrictor systems. (HEPATOL-OGY 1998;28:39-44.)Portal hypertension in cirrhosis is associated with a hyperdynamic circulation, which is characterized by hypervolemia, high cardiac output, arterial hypotension, and low peripheral vascular resistance. 1 These circulatory abnormalities are thought to be secondary to a splanchnic arteriolar vasodilation related to the increase in portal pressure. Portal hypertension in experimental animals is associated with a generalized splanchnic arteriolar vasodilation. 2,3 There is indirect evidence that this also occurs in human cirrhosis, as hepatic blood flow is usually normal or increased in these patients, even though 60% to 80% of portal flow is shunted through the collateral circulation. 4 In addition, the mean transit time in the splanchnic vascular bed is substantially reduced in alcoholic cirrhotic patients, which indicates a hyperkinetic splanchnic circulation in these patients. 5 Finally, studies using echo-Doppler have documented increased splenic and mesenteric blood flow in patients with cirrhosis. 6,7 Investigations assessing regional circulations in human cirrhosis are also consistent with that concept. Renal blood flow is reduced and renal vascular resistance is increased in most patients with cirrhosi...

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“…17,18 Consequently, renal perfusion pressure is reduced, leading to decreased renal blood flow. 19 Compensatory activation of various vasoconstrictor systems maintains hemodynamic stability, whereas vasoconstriction occurs in some nonsplanchnic vascular beds including the kidneys, 20 thereby further reducing renal perfusion with consequent reduction in glomerular filtration rate. 21 However, two patients with similarly reduced renal blood flow may or may not have HRS.…”

Section: The Pathophysiology Of Hrs and Its Role In Preventionmentioning

confidence: 99%

New challenge of hepatorenal syndrome: Prevention and treatment

Wong¹

2001

Hepatology

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Hepatorenal syndrome (HRS) remains one of the major therapeutic challenges in hepatology today. The pathogenesis is complex, but the final common pathway seems to be that sinusoidal portal hypertension, in the presence of severe hepatic decompensation, leads to splanchnic and systemic vasodilatation and decreased effective arterial blood volume. Renal vasoconstriction increases concomitantly, renal hemodynamics worsens, and renal failure occurs. Renal failure was shown 15 years ago to be potentially reversible after liver transplantation. This potential reversibility together with increased understanding of the pathogenesis has led to successful preliminary attempts to reverse HRS nonsurgically with combinations of splanchnic vasoconstrictors and colloid volume expansion, insertion of transjugular intrahepatic portovenous shunt radiologically, and improved forms of dialysis. Recent classification of HRS into the acute onset or severe type 1 with virtually 100% mortality and the more insiduous less severe type II promises to shed more light on the pathogenesis of HRS, especially on the currently unrecognized precipitating factors. It is hoped that this classification will be included in the necessary and carefully performed clinical trials, which should lead to clearer indications for the available therapies. The challenge now is to use all this information to improve our management of cirrhotic patients to prevent occurrence of HRS in the future. (HEPATOLOGY 2001;34:1242-1251.)Progressive oliguric renal failure is a common and severe complication in patients with advanced liver disease. In a large prospective follow-up study of cirrhotic patients with ascites, development of renal failure occurred in 18% and 39% of the patients at 1 year and at 5 years, respectively, with a median survival of 1.7 weeks or a 90% mortality at 10 weeks. 1 Hepatorenal syndrome (HRS) originally referred to occurrence of renal failure following biliary surgery. 2 The definitions of HRS gradually evolved to describe the renal failure observed in patients with liver failure associated with low urinary sodium levels and absence of renal pathology. 3 A recent consensus conference further defined HRS as types I and II with the following diagnostic criteria: type I HRS is characterized by rapidly progressive renal failure with a doubling of serum creatinine to a level greater than 2.5 mg/dL or a halving of the creatinine clearance to less than 20 mL/min in less than 2 weeks; type II HRS is a more chronic form with a slowly progressive increase in serum creatinine level to greater than 1.5 mg/dL or a creatinine clearance of less than 40 mL/min 4 and has a corresponding better prognosis. Until recently, liver transplantation was the only definitive treatment for HRS. 5,6 However, even then, the reported survival rates of these HRS patients posttransplantation have been less than in transplanted patients with normal renal function, and the return of renal function to normal may be delayed for months or years. 7,8 Furthermore, liver transplanta...

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Brachial and femoral artery blood flow in cirrhosis: Relationship to kidney dysfunction

Cited by 71 publications

References 31 publications

Clinical implications of the hyperdynamic syndrome in cirrhosis

Clinical implications of the hyperdynamic syndrome in cirrhosis

Increased cerebrovascular resistance in cirrhotic patients with ascites

New challenge of hepatorenal syndrome: Prevention and treatment

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