Sodium overload

Patients with sodium overload should be treated with loop diuretics (furosemide, 20 to 40 mg IV every 6 hours) and 5% dextrose at a rate that decreases serum sodium by approximately 0.5 mEq/L/hour or, if hypernatremia developed rapidly, 1 mEq/L/hour. 

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications. 

It is a tuberculostatic and very less active drug in the treatment of tuberculosis. It is used as sodium salt and its larger dose can cause sodium overload in the body. 

Bicarbonate, sodium Membrane-depressant cardiotoxic drugs (tricyclic antidepressants, quinidine, etc) 1-2 mEq/kg IV bolus usually reverses cardiotoxic effects (wide QRS, hypotension). Give cautiously in heart failure (avoid sodium overload). 

This mechanism is thought to be the basis of the therapeutic effect of this compound in cardiac ischemia, since one of the main causes of arrhythmia in this condition is attributable to sodium overload. 

These are adapted from the ampicillin molecule, with a side-chain derived from urea. Their major advantages over the carboxypenicillins are higher efficacy against Pseudomonas aeruginosa and the fact that as monosodium salts they deliver on average about 2 mmol of sodium per gram of antimicrobial (see above) and are thus safer where sodium overload should particularly be avoided. They are degraded by many p-lactamases. Ureidopenicillins must be administered parenterally and are eliminated mainly in the urine. Accumulation in patients with poor renal function is less than with other penicillins as 25% is excreted in the bile. An unusual feature of their kinetics is that, as the dose is increased, the plasma concentration rises disproportionately, i.e. they exhibit saturation (zero-order) kinetics. 

Some 65% of the filtered sodium is actively transported from the lumen of the proximal tubule by the sodium pump (Na", K -ATPase). Chloride is absorbed passively, accompan)dng the sodium bicarbonate is also absorbed, through the action of carbonic anhydrase. These solute shifts give rise to the iso-osmotic reabsorption of water, with the result that > 70% of the glomerular filtrate is returned to the blood from this section of the nephron. The epithelium of the proximal tubule is described as leaky because of its free permeability to water and a number of solutes. Osmotic diuretics such as mannitol are solutes which are not reabsorbed in the proximal tubule (site 1. Fig. 26.1) and therefore retain water in the tubular fluid. Their effect is to increase water rather than sodium loss, and this is reflected in their special use acutely to reduce intracranial or intraocular pressure and not states associated with sodium overload. 

Oedema states associated with sodium overload, e.g. cardiac, renal or hepatic disease, and also without sodium overload, e.g. acute pulmonary oedema following myocardial infarction. Note that oedema may also be localised, e.g. angioedema over the face and neck or aroimd the ankles following some calcium channel blockers, or due to low plasma albumin, or immobility in the elderly in none of these circumstances are diuretics indicated. 

In hyperkalaemia, oral administration or retention enemas of a polystyrene sulphonate resin may be used. A sodium phase resin (Resonium A) should obviously not be used in patients with renal or cardiac failure as sodium overload may result. A calcium phase resin (Calcium Resonium) may cause hypercalcaemia and should be avoided in predisposed patients, e.g. those with multiple myeloma, metastatic carcinoma, hyperparathyroidism and sarcoidosis. Enemas should be retained for as long as possible, although patients rarely manage for... 

The urine can be made alkaline by sodium bicarbonate i.v., or by potassium citrate by mouth. Sodium overload may exacerbate cardiac failure, and sodium or potassium excess are dangerous when renal function is impaired. 

Sodium bicarbonate is metabolized to the sodium cation, which is eliminated from the body by renal excretion, and the bicarbonate anion, which becomes part of the body s bicarbonate store. Any carbon dioxide formed is eliminated via the lungs. Administration of excessive amounts of sodium bicarbonate may thus disturb the body s electrolyte balance, leading to metabolic alkalosis or possibly sodium overload with potentially serious consequences. The amount of sodium present in antacids and effervescent formulations has been sufficient to exacerbate chronic heart failure, especially in elderly patients. ... 

Potassium bicarbonate No possibility of sodium overload used as an alternative to sodium bicarbonate in some preparations Hyperkalaemia possible with prolonged regular use in patients taking potassiumsparing diuretics or angiotensinconverting enzyme inhibitors... 

Treatment of sodium overload consists of administration of loop diuretics to facilitate excretion of the excess sodium, as well as intravenous D5W. The latter should be infused at a rate that will decrease the serum sodium at approximately 0.5 mEq/L per hour, or 1 mEq/L per hour in cases in which the hypernatremia developed rapidly over several hours. ° The volume of infusate may be estimated as described previously. Furosemide should be administered at a dose of 20 to 40 mg intravenously every 6 hours. 

Hyponatraemic patients with oedema are likely to have both water and sodium overload. These patients may be treated with diuretics and fluid restriction. 

Water and sodium intake should be carefully matched to the losses. Dietary sodium restriction and diuretics may be required to prevent sodium overload. 

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