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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bumetanide and frusemide were compared in a crossover study of 10 patients with cirrhosis and fluid overload. Patients received each drug for 3 months. Doses of bumetide varied from 1 mg on alternate days to 3 mg daily (mean 1.3 mg/day), and for frusemide from 40 mg on alternate days to 160 mg daily (mean 72 mg/day). Both drugs proved effective in controlling ascites and oedema, 9 out of the 10 patients showing a satisfactory response. Minor side-effects, hypokalaemia and hyperuricaemia were common with both agents, and hypomagnesaemia and metabolic alkalosis developed in some patients.
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PMID:Treatment of fluid retention in cirrhosis: a comparison of bumetanide and frusemide. 33 56

Several hemodynamic abnormalities in the patient with cirrhosis comprise a unique distributive circulatory disturbance that causes intractable ascites and that is, in turn, worsened by the resulting ascites. Ascites is promptly alleviated by drainage of the ascitic fluid into the intravascular compartment. The circulatory abnormalities improve in part because of elimination of the ascites, and also because of a compensatory hypervolemia. The consequences of the latter, especially in the immediate postoperative period, are increased likelihood of pulmonary edema and of gastrointestinal bleeding from heightened portal vein pressure. Postoperative coagulopathy is also a significant problem. Careful selection of patients for the procedure, close postoperative observation and vigorous use of diuretics and other agents will usually enable these complications to be obviated or successfully treated. Increases in body muscle and fat masses and serum albumin concentrations indicate nutritional improvement. Despite evidence of benefits from the procedure, these patients continue to die from the complications that threaten other cirrhotics: effects of return to alcoholism, gastrointestinal hemorrhage, recurrent infections and intestinal obstruction. Thus, it is not yet clear that the benefits include prolongation of life.
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PMID:Treatment of intractable ascites in patients with alcoholic cirrhosis by peritoneovenous shunting (LeVeen). 44 38

Morphological examinations of 24 autopsy cases of liver cirrhosis demonstrated the development of secondary postcapillary pulmonary hypertension with an increase of the muscular mass of the right ventricle and rearrangement of the blood vessels of pulmonary circulation. Most important morphological changes were observed in intraorgan veins and microcirculatory bed of the visceral pleura (particularly in the venular knee) indicating early reaction of the veins to hemodynamic disorders. It is suggested that hypervolemia in the pulmonary circulation system developing at the expence of blood discharge from the portal system into direct portopulmonary anastomoses plays an important role in the genesis of pulmonary hypertension in patients with hepatic cirrhosis.
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PMID:[Morphological characteristics of secondary pulmonary hypertension in liver cirrhosis]. 45 26

Morphological examinations of the microcirculatory bed of the lungs and pulmonary pleura in 30 fatal cases of cirrhosis of the liver revealed generalized involvement of the blood and lymph vessels. Most significant changes were found in venular and lymphomicrocirculatory parts of the pulmonary pleura as a manifestation of compensatory-adaptative processes directed at retention of the hemodynamic homeostasis of the pulmonary circulation. In the author's opinion, the most important factors causing reactions of the microcirculatory bed of the pulmonary pleura include venous hypervolemia of the pulmonary circulation followed by hypoxia. It is suggested that changes in the vessels of the microcirculatory bed of the lungs and pulmonary pleura in patients with cirrhosis of the liver are an important part of the compensatory-adaptative mechanisms; their disorders cause the development of the right ventricle insufficiency.
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PMID:[Morphology of the microcirculatory bed of the lungs and visceral pleura in liver cirrhosis]. 74 93

Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI) results in a significant natriuresis, kaliuresis, and diuresis. The NI model was utilized to assess the role of "effective volume" and hyperaldosteronism in the impairment of sodium and water handling in cirrhosis. Eleven cirrhotic patients were studied twice while in balance on a 10 mEq. Na, 100 mEq. K diet: control and NI. The conditions of seated posture and time of day were identical. UNaV was constant throughout C, ranging from 1 to 2 muEq per minute. During NI, UNaV increased progressively from 1 +/- 1 (S.E.M.) during the prestudy hour to 89 +/- 32 muEq per minute during hour 5 of NI (p less than 0.02), greatly exceeding the comparable value found in normal subjects on an identical diet. (See article).
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PMID:Determinants of deranged sodium and water homeostasis in decompensated cirrhosis. 127 Aug 90

To assess the hemodynamic status of patients with compensated cirrhosis, mean arterial pressure, cardiac index and peripheral vascular resistance and markers of central (plasma concentrations of atrial natriuretic factor) and arterial volemia (plasma norepinephrine concentration, plasma renin activity) were studied in 10 patients and 10 healthy control subjects under steady-state conditions (after 2 hr of standing) and after assumption of the supine position (30, 60, and 120 min). After standing, neither hemodynamics nor markers of effective volemia differed significantly between controls and patients. By evaluating the areas under the curve during the 2 hr of supine posture, the increase in cardiac output and plasma natriuretic factor and the decrease in peripheral vascular resistance were greater in patients (2.59 +/- 0.43 [S.E.M.] L/min/hr; 32.8 +/- 7.2 pg/ml/hr -1,103 +/- 248.4 dyn.sec/cm5/hr, respectively) than in controls (0.53 +/- 0.24 L/min/hr, p = 0.005; 17.4 +/- 4.7 pg/ml/hr, p = 0.005; -265.5 +/- 206.2 dyn.sec/cm5/hr, p = 0.02). The declines in heart rate, plasma norepinephrine concentration and plasma renin activity did not differ significantly. Mean arterial pressure did not significantly change. Our results suggest that during periods of upright posture, cirrhotic patients in the preascitic stage, who are known to have expanded blood volume, compensate for dilatation of the splanchnic vascular bed through total hypervolemia. The latter becomes excessive during recumbency, leading to supernormal increases in venous return, central volemia and cardiac index. The decline in peripheral vascular resistance appears to be a compensatory mechanism to maintain steady arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The hemodynamic status of preascitic cirrhosis: an evaluation under steady-state conditions and after postural change. 138 33

This study assessed the validity of bioelectrical impedance analysis (BIA) to predict total body water (TBW) in patients with cirrhosis. TBW was estimated by deuterium oxide dilution (D2O) and compared with TBW predicted by BIA in 27 patients with cirrhosis with and without ascites or edema (Group A), in a subgroup of 18 'dry' cirrhotics without clinical signs of fluid overload (Group B) and in 27 healthy controls. Three different BIA regression equations were used. In all three groups of subjects high correlation coefficients were obtained between D2O-TBW and BIA-TBW (r > 0.88). In the cirrhotic Group A, BIA significantly underpredicted D2O-TBW by all 3 equations (2.9-3.8 l) and the regression lines were different from the lines of identity by two equations. Standard errors of estimate were high in Group A (3.04-3.97 l) in comparison with Group B (1.79-2.46 l) and the controls (1.03-1.41 l). In the 'dry' cirrhotics (Group B) and in the controls, TBW was correctly predicted by two of three BIA equations, and regression lines were not significantly different from lines of identity. Correlation coefficients in Group B were higher than in Group A (r = 0.96-0.97 vs. 0.89-0.92) and were comparable with controls (r = 0.98-0.99). We conclude that BIA is not a valid method of estimating TBW in cirrhotic patients with ascites and edema. In cirrhotic patients without clinical signs of fluid overload BIA can be used to predict TBW, although accuracy is slightly lower than in healthy controls.
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PMID:The validity of bioelectrical impedance analysis in estimating total body water in patients with cirrhosis. 148 69

HRS occurs frequently in patients with advanced cirrhosis of the liver and fulminant hepatitis. The pathogenesis of HRS is not clearly understood; reduced effective plasma volume and intense renal cortical vasoconstriction seem to have important roles. The HRS is a diagnosis by exclusion, and it [table: see text] is often difficult to differentiate this entity from prerenal azotemia and ATN. The HRS is characterized by its relentless progression and usually fatal outcome. The essential steps in the management of HRS are to identify and correct the precipitating factors leading to HRS and avoidance of potential hepatotoxic and nephrotoxic drugs. Patients with potentially reversible liver diseases should be treated aggressively. Volume expansion is important and should be tried first, even though hypovolemia may be not clinically evident. Dialysis may benefit patients with fluid overload and electrolyte imbalance or those awaiting liver transplantation. In selective cases, peritoneovenous shunt may be of value. Liver transplantation is the only curative therapy available at present.
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PMID:The hepatorenal syndrome. 219 63

A 41-year-old hemodialyzed woman developed ascites and was found to have secondary iron overload. The dose of administered iron was approximately 11-12 g, and her serum ferritin level was 15,000 ng/ml (15,000 micrograms/l). There were no signs of congestive heart failure, fluid overload, or liver cirrhosis. A program of weekly phlebotomy combined with recombinant human erythropoietin (rhEPO) therapy was tried to eliminate the iron congestion. After 9 months of this therapy, about 5 g of iron had been removed. The ascites completely disappeared, and her serum ferritin level fell to 5,800 ng/ml (5,800 micrograms/l). This suggests that such combined therapy would be useful when iron overload must be corrected rapidly. Before therapy, the sterile ascitic fluid showed exudative characteristics with 3.7 g/dl (37 g/l) of total protein. The serum-ascites albumin difference was 0.6 g/dl (6 g/l), and the fluid contained 1,400 inflammatory cells/mm3 (1.4 X 10(9)/l). Notably, the serum-ascites albumin difference increased in parallel with iron elimination. These findings suggested that iron deposition may have played a role in changing the permeability of the peritoneum, or in impairing lymphatic drainage, both of which are presumed to be pathogenetic factors of nephrogenic ascites.
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PMID:Treatment of a patient with end-stage renal disease, severe iron overload and ascites by weekly phlebotomy combined with recombinant human erythropoietin. 236 36

The results of the study showed that the cardiovascular system of patients with hepatic cirrhosis and ascites tolerate acute hypervolemia better than patients with hepatic cirrhosis without ascites. It can be explained by a rapid transfer of surplus liquid into the abdominal cavity. Further, it was found that the low cardiac output at rest in patients with hepatic cirrhosis evidently indicated a latent cardiac insufficiency becoming manifest only after the volume exertion. In our control group, jaundice produced bradycardia and hypotension without cardiodepressive effects. Patients with cirrhosis and with or without ascites responded to furosemide probably associated with the elution of vasoconstrictive substances in the same way as the control group. Following acute volume expansion, no differences were found between the compensated and decompensated cirrhotic patients and the healthy control group, not even in the natriuretic hormone of the secretion. However, the relevant organs of each control group had a varied response to the elevated plasma level of natriuretic factor.
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PMID:[Reaction of the cardiovascular and humoral system to acute hypervolemia in patients with liver cirrhosis]. 252 57


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