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Sodium restriction

Dietary sodium restriction Reduce dietary sodium intake to no more than 100 mmol per day (2.4 g sodium or 6 g sodium chloride) 2-8 mm Hg... [Pg.16]

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. [Pg.330]

Diuretics are often required in addition to the sodium restriction described previously. Spironolactone and jurosemide form the basis of pharmacologic therapy for ascites. Spironolactone is an aldosterone antagonist and counteracts the effects of activation of the renin-angiotensin-aldosterone system. In hepatic disease not only is aldosterone production increased, but its half-life is prolonged because it is hepatically metabolized. Spironolactone acts to conserve the potassium that would be otherwise excreted because of elevated aldosterone levels. [Pg.332]

Measure spot urine sodium/potassium ratio to assess adherence to dietary sodium restrictions. [Pg.335]

Provide education regarding dietary sodium restrictions at each visit consider a referral to a dietician if appropriate. [Pg.335]

The kidney is unable to adjust to abrupt changes in sodium intake in patients with severe CKD. Therefore, patients should be advised to refrain from adding salt to their diet, but should not restrict sodium intake. Changes in sodium intake should occur slowly over a period of several days to allow adequate time for the kidney to adjust urinary sodium content. Sodium restriction produces a negative sodium balance, which causes fluid excretion to restore sodium balance. The resulting volume contraction can decrease perfusion of the kidney and hasten the decline in GFR. Saline-containing intravenous (IV) solutions should be used cautiously in patients with CKD because the salt load may precipitate volume overload. [Pg.381]

In order to achieve a goal blood pressure, lifestyle modifications, including diet, exercise, sodium restriction, and smoking cessation, are recommended.63 Unfortunately, lifestyle modifications alone often are inadequate to control HTN in this high-risk population, and antihypertensive medications usually are needed. [Pg.848]

The mainstay of treatment for established SOS is supportive care aimed at sodium restriction, increasing intravascular volume, decreasing extracellular fluid accumulation, and minimizing factors that contribute to or exacerbate hepatotoxicity and encephalopathy. Defibrotide has shown promising results in the treatment of SOS.44... [Pg.1455]

Compensatory mechanisms in HF stimulate excessive sodium and water retention, often leading to systemic and pulmonary congestion. Consequently, diuretic therapy (in addition to sodium restriction) is recommended in all patients with clinical evidence of fluid retention. However, because they do not alter disease progression or prolong survival, they are not considered mandatory therapy for patients without fluid retention. [Pg.98]

All patients with prehypertension and hypertension should be prescribed lifestyle modifications, including (1) weight reduction if overweight, (2) adoption ofthe Dietary Approaches to Stop Hypertension eating plan, (3) dietary sodium restriction ideally to 1.5 g/day (3.8 g/day sodium chloride), (4) regular aerobic physical activity, (5) moderate alcohol consumption (two or fewer drinks per day), and (6) smoking cessation. [Pg.126]

The treatment of ascites secondary to portal hypertension includes abstinence from alcohol, sodium restriction, and diuretics. Sodium chloride should be restricted to 2 g/day. [Pg.259]

Several factors predispose to lithium toxicity, including sodium restriction, dehydration, vomiting, diarrhea, drug interactions that decrease lithium clearance, heavy exercise, sauna baths, hot weather, and fever. Patients should be told to maintain adequate sodium and fluid intake and to avoid excessive coffee, tea, cola, and other caffeine-containing beverages and alcohol. [Pg.789]

The kidney s ability to adjust to abrupt changes in sodium intake is diminished in patients with ESRD. Sodium restriction beyond a no-added-salt diet is not recommended unless hypertension or edema is present. A negative sodium balance can decrease renal perfusion and cause a further decline in GFR. [Pg.877]

Patients with nephrogenic DI should decrease their ECF volume with a thiazide diuretic and dietary sodium restriction (2,000 mg/day), which often decreases urine volume by as much as 50%. Other treatment options include drugs with antidiuretic properties (Table 78-2). [Pg.897]

Pulmonary edema requires immediate pharmacologic treatment. Other forms of edema can be treated gradually with, in addition to diuretic therapy, sodium restriction and correction of underlying disease state. [Pg.898]

International Society of Thrombosis and Haemostasis (ISTH), 12 151 International Society of Hypertension, on sodium restriction, 22 813 International Solvent Extraction Conferences (ISEC), 10 746, 766 International Standard (ISO) 2370, for flax fiber, 11 614, 616, 617... [Pg.483]

World gold reserves, 12 686 World Health Organization (WHO), 18 541 safe cities and safe communities programs of, 24 183 on sodium nitrate, 22 849-850, 851 on sodium restriction, 22 813 World Intellectual Property Office,... [Pg.1025]

Excessive vitamin C doses Diabetics, patients prone to recurrent renal calculi, those undergoing stool occult blood tests and those on sodium restricted diets or anticoagulant therapy should not take excessive doses of vitamin C over an extended time period. [Pg.5]

Preparations containing sodium should be used cautiously by individuals on a sodium-restricted diet, and in the presence of edema, CHF, renal failure, or borderline hypertension. [Pg.1409]

Sodium-restricted diets Each buffered tablet contains 264.5 mg sodium. Each single-dose packet of buffered powder for oral solution contains 1380 mg sodium. Hyperuricemia Didanosine has been associated with asymptomatic hyperuricemia consider suspending treatment if clinical measures aimed at reducing uric acid levels fail. [Pg.1848]

Sodium restriction is essential to control the edema. Diuretics like thiazides or loop diuretics are indicated in patients who are symptomatic from the edema. [Pg.615]

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. [Pg.631]

Dietary sodium restriction has been known for many years to decrease blood pressure in hypertensive patients. With the advent of diuretics, sodium restriction was thought to be less important. However, there is now general agreement that dietary control of blood pressure is a relatively nontoxic therapeutic measure and may even be preventive. Even modest dietary sodium restriction lowers blood pressure (though to varying extents) in many hypertensive persons. [Pg.226]

Weight reduction even without sodium restriction has been shown to normalize blood pressure in up to 75% of overweight patients with mild to moderate hypertension. Regular exercise has been shown in some but not all studies to lower blood pressure in hypertensive patients. [Pg.241]

When given in larger than physiologic amounts, steroids such as cortisone and hydrocortisone, which have mineralocorticoid effects in addition to glucocorticoid effects, cause some sodium and fluid retention and loss of potassium. In patients with normal cardiovascular and renal function, this leads to a hypokalemic, hypochloremic alkalosis and eventually to a rise in blood pressure. In patients with hypoproteinemia, renal disease, or liver disease, edema may also occur. In patients with heart disease, even small degrees of sodium retention may lead to heart failure. These effects can be minimized by using synthetic non-salt-retaining steroids, sodium restriction, and judicious amounts of potassium supplements. [Pg.885]

DOC, which also serves as a precursor of aldosterone (Figure 39-1), is normally secreted in amounts of about 200 mcg/d. Its half-life when injected into the human circulation is about 70 minutes. Preliminary estimates of its concentration in plasma are approximately 0.03 mcg/dL. The control of its secretion differs from that of aldosterone in that the secretion of DOC is primarily under the control of ACTH. Although the response to ACTH is enhanced by dietary sodium restriction, a low-salt diet does not increase DOC secretion. The secretion of DOC may be markedly increased in abnormal conditions such as adrenocortical carcinoma and congenital adrenal hyperplasia with reduced P450cll or P450cl7 activity. [Pg.887]

Diuretics lower blood pressure primarily by depleting body sodium stores. Initially, diuretics reduce blood pressure by reducing blood volume and cardiac output peripheral vascular resistance may increase. After 6-8 weeks, cardiac output returns toward normal while peripheral vascular resistance declines. Sodium is believed to contribute to vascular resistance by increasing vessel stiffness and neural reactivity, possibly related to increased sodium-calcium exchange with a resultant increase in intracellular calcium. These effects are reversed by diuretics or sodium restriction. [Pg.231]

The initial step in treating hypertension may be nonpharmacologic. As discussed previously, sodium restriction may be effective treatment for many patients with mild hypertension. The average American diet contains about 200 mEq of sodium per day. A reasonable dietary goal in treating hypertension is 70-100 mEq of sodium per day, which can be achieved by not salting food... [Pg.254]


See other pages where Sodium restriction is mentioned: [Pg.185]    [Pg.471]    [Pg.640]    [Pg.173]    [Pg.16]    [Pg.16]    [Pg.43]    [Pg.51]    [Pg.98]    [Pg.868]    [Pg.860]    [Pg.615]    [Pg.226]    [Pg.226]    [Pg.238]    [Pg.241]    [Pg.341]    [Pg.300]    [Pg.250]    [Pg.374]   


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