Ascites salt restriction

If tense ascites is present, a 4- to 6-L paracentesis should be performed prior to institution of diuretic therapy and salt restriction. 

When diuretics are administered at the same time, it is not absolutely necessary to adhere to strict salt restriction. We followed the recommended 6-8 g/day. Indeed, such a moderate restriction is usually observed more reliably by the patient. Reducing water intake to 1.5-2.0 1/day is also sufficient. Only a hyponatraemic condition of <130 mmol/1 requires a reduction in fluid intake to <1,000 ml/day. Determination of fractional sodium elimination (FEnJ may point to potential success even before treatment has begun with a value of >0.5%, treatment steps 1 and 2 (see above) will achieve a probable success rate of about 95%. This favourable initial situation is supported by a still sufficient spontaneous sodium excretion of >40 mmol/day. Therapy resistance must be anticipated when fractional sodium elimination is <0.1% and sodium excretion is <10 mmol/day. If treatment steps 1—4 are unsuccessful or renal function is clearly impaired initially and FENa is <0.1%, the insertion of a peritovenous shunt (PVS) should be considered. This procedure is designed to make use of the principle of ascites reinfusion for as long as possible, (s. tabs. 16.14—16.18) (s. p. 311) TIPS may also prove to be an alternative to PVS, especially when using a polytetrafluoroethylene-covered stent to prevent occlusion. (Ill) (s. fig. 16.15) (s. pp 259, 314, 362)... 

In adult patients with new-onset ascites as determined by physical exam or radiographic studies, abdominal paracentesis should be performed and ascitic fluid analysis should include a cell count with differential and a serum-ascites albumin gradient (SAG). If infection is suspected, ascitic fluid cultures should be obtained at the time of the paracentesis. The SAG can accurately determine whether ascites is a result of portal hypertension or another process. If the SAG is >1.1 g/dL, portal hypertension is present with 97% accuracy. If the SAG is <1.1 g/dL, with similar certainty the patient does not have portal hypertension. This is important because patients without portal hypertension will not respond to salt restriction and diuretics. The treatment of ascites secondary to portal hypertension is relatively straightforward and includes abstinence from alcohol, sodium restriction, and diuretics. This strategy is effective in approximately 90% of patients. Fifteen percent of patients will respond to dietary sodium restriction alone, and an additional 75% of patients will respond to the addition of diuretics. ... 

Beyond avoidance of alcohol, the primary treatment is salt restriction and oral diuretic therapy. Achieving the desired fluid losses in patients with ascites caused by portal hypertension is directly related to sodium balance, not fluid restriction. To monitor these patients, evaluation of urinary sodium excretion, utilizing a 24-hour urine collection, is recommended. However, severe hyponatremia, serum sodium <120 mEq/L, does warrant fluid restriction rapid correction of asymptomatic hyponatremia (patients with cirrhosis usually are not symptomatic until their serum sodium concentrations are <110 mEq/L) is not recommended. 

A 10-yr-old British boy was diagnosed with Crohn s disease and was treated with an herbal tea containing comfrey leaf. Other medications included sporadic use of prednisolone and sulfasalazine. Three years later, he presented with weight loss, diarrhea, fever, abdominal pain, ascites, tender hepatomegaly, and fatigue. Laboratory tests revealed mild iron deficiency anemia (Hgb 117 g/L), elevated bilirubin (26 mmol/L) and aspartate aminotransferase level (87 IU/L), and low serum albumin. Ascitic fluid protein concentration was 27 g/L. Liver biopsy showed the thrombotic variant of venoocclusive disease. He was treated with salt restriction and spironolactone, with good response. 

In a subsequent study, 5 patients were receiving AmB in clinical situations where salt-conserving states could be identified. These included dietary salt restriction, vomiting, diuretic therapy, Addison s disease and cirrhosis with ascites. In each patient sustained increases in BUN and serum creatinine levels were observed within 6 to 12 days after starting AmB [108]. 

All patients with ascites require counseling on dietary sodium restriction. Salt intake should be limited to less than 800 mg sodium (2 g sodium chloride) per day. More stringent restriction may cause faster mobilization of ascitic fluid, but adherence to such strict limits is very difficult. Patients usually respond well to sodium restriction accompanied by diuretic therapy.14,22,31,32 The goal of therapy is to achieve urinary sodium excretion of at least 78 mEq (78 mmol) per day.22 While a 24-hour urine collection provides this information, a spot urine sodium/ potassium ratio greater than 1.0 provides the same information and is much less cumbersome to perform. 

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. 

Elimination of hyponatraemia (<125 mmol/1) is extremely difficult. In this case, the overall status of body sodium is increased, and hence the body fluid as well, whereas the sodium level in the serum is lowered (= dilutional hyponatraemia). Treatment is effected by strictly limiting the intake of fluid (<700-900 ml/day) and rigidly restricting salt. Should these measures fail to raise sodium levels in the serum and increase diuresis, intravenous administration of a hypertonic sodium chloride solution (3%) can be attempted (increasing serum sodium by no more than 1-1.5 mmol/1 per hour and, if possible, never in excess of 130 mmol/1). This, however, automatically harbours the danger of tense ascites. For this reason, an i.v. application of furosemide should be given at the same time to promote the clearance of free... 

Ascites The oeeurrence of a disturbed water-eleetrolyte balance in the late stage of latent oedema (s. fig. 15.3) (s. p. 297) requires immediate restriction of the salt intake (<3-6 g/day) - depending on the level of natriuresis the intake of fluid is limited to 1.0 (-1.5) 1/day especially in hyponatriaemia. An intermittent fruit and rice diet (generally for 1-2 days) is recommended because it is extremely low in sodium, but rich in potassium. Marked NaCl restriction simultaneously leads to a reduction in protein intake. The use of commercially available low-salt protein preparations is therefore advisable (e.g. 60 g protein/100 g + 5 mval sodium/100 g, or 48 g protein/100 g + 13 g, or 15 g sodium/100 g). 

Patients with severe cirrhosis often have ascites and peripheral edema. The excess of total body sodium in the presence of an even greater excess of total body water results in hyponatremia. Salt and fluid restrictions are required in order to avoid exacerbating this overhydrated state (see Chap. 49). Caution must be exercised, however, because severe sodium and fluid restriction may result in intravascular depletion, which may cause or exacerbate hepatic encephalopathy. 

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