Plasma sodium

When plasma glucose falls to <250 mg/dL, switch to D5W, D5W/half NS, or D5W/NS depending on plasma sodium concentration... 

Qi, X. 1., Huang, Y., Wang, Y. Q. et al. (2004). Association of plasma sodium phenytoin concentration with CYP2C19 gene polymorphism. Chinese Journal of New Drugs, 13( 10), 922-5. 

Chemistry Plasma urea Plasma sodium Plasma potassium Plasma creatinine... 

These results suggest acute renal failure (ARF) due to tubular necrosis caused by phenol. Plasma sodium is low due mainly to impaired reabsorption in the nephron, although the slightly low albumin suggests haemodilution possibly as a result of excessive i.v. fluids. Potassium is raised due to poor exchange with sodium in the distal tubule and the acidosis (low pH and low bicarbonate concentration) arises from defective acidification of the glomerular filtrate acidosis is often associated with hyperkalaemia (raised plasma... 

The mainstay of medical treatment is fluid restriction, but this may not be appropriate in the surgical and critical care patient population. Severe (<120 mmol-L-l) or symptomatic hyponatraemia (mental status changes, seizure) requires more aggressive therapy to reduce cerebral oedema. Infusion of hypertonic saline to increase plasma sodium concentrations to 120-125 mmol L-1 alleviates symptoms. Adjunct therapy with demeclocycline (600 mg-day-1) may assist management in resistant SIADH. Demeclocycline is a tetracycline antibiotic which inhibits the actions of ADH at the renal tubules. 

Sweat is not just water but a dilute solution of electrolytes, mainly sodium and chloride. The actual composition varies from individual to individual and within individuals, according to circumstances. Typical values are shown in Table 13.6, from which it can be seen that sweat is considerably less concentrated than plasma. Hence sweating causes an increase in plasma electrolyte concentrations. Only in events of long duration (more than 3 h) is it considered essential to replace lost sodium during the event to guard against hyponatraemia (low plasma sodium concentration) (Gisolfi and Duchman, 1992). However, sports drinks conventionally contain added sodium, chloride and other electrolytes at levels similar to those found in sweat. 

In 70 non-insulin-dependent patients with diabetes, taking one of five different oral hypoglycemic drugs, 21% of prescriptions were associated with a low plasma sodium concentration, but it was lower than 129 mmol/1 in only 8% (75). Every oral hypoglycemic agent was associated with a low plasma sodium concentration, which normalized on withdrawal. Extreme hyponatremia was only seen with chlorpropamide and, in one case, with glibenclamide. 

In a double-blind, crossover study, 20 men aged 52-80 years were given desmopressin for nocturia. Three of them had symptoms due to fluid retention, particularly bloating, headache, and reversible weight gain, and two of these had a significant fall in plasma sodium (53). In a meta-analysis of 14 studies of serum sodium in 529 patients treated with desmopressin there was mild asymptomatic hyponatremia in up to 10% of patients (54). 

Fluid balance and plasma electrolytes should be monitored to prevent this complication, particularly if repeated doses are required. Children seem to be particularly vulnerable to this complication (55). In a longterm, open study of 245 Swedish children given intranasal desmopressin 20-40 micrograms at night for enuresis, five had an asymptomatic fall in plasma sodium (36). Mild hyponatremia, which did not cause symptoms, was found in five of 399 children in an open, multicenter trial (56). 

A 13 kg 3-year-old boy given 40 micrograms of desmopressin intravenously and 1.6 liters of hypotonic fluid over 12 hours had convulsions and a respiratory arrest his plasma sodium fell to 114 mmol/1 (58). 

In mild cases of hyponatremia, treatment typically focuses on water restriction (< 800 mL/day) however this approach suffers from poor patient compliance due to thirst brought on by increasing serum osmolality.1,10 In cases of extreme hyponatremia, infusions of hypertonic saline are used to elevate serum sodium concentrations. Loop diuretics (e.g., furosemide) are often used as an adjunct to such treatment to offset potential volume overload.1 Hypertonic saline therapy is also suboptimal, as it carries a risk of overly rapid adjustment of plasma sodium levels, which can result in the rapid shift of water from brain tissue to the vascular space, triggering neural demyelination that can result in seizures, coma, quadriplegia, and even death.1... 

Because of the serious risks involved in long-term lithium treatment, patients plasma levels are reassessed regularly, usually every three months. If plasma lithium concentration becomes too high, administration of the drug is suspended and large amounts of sodium salts and fluids are given. Since lithium toxicity is enhanced by sodium depletion, the increased plasma sodium and fluids can reduce its toxic effects. 

Q4 Potassium concentration is mainly controlled by the steroid hormone aldosterone. Aldosterone release from the adrenal cortex can be stimulated by either decreased plasma sodium or by increased plasma potassium concentration. An increase in aldosterone secretion causes retention (reabsorption) of sodium in the distal nephron in exchange for secretion of potassium into the urine. The amount of potassium excreted by the kidney is influenced by the acid-base status of the body. In alkalosis, potassium excretion increases, whereas in acidosis it is decreased. In the distal nephron H+ and K+ compete for excretion in exchange for the reabsorption of sodium. Insulin also affects plasma potassium concentration because it promotes the movement of potassium from the plasma into cells. 

Control of plasma sodium and potassium concentration by aldosterone... 

A 47-year-old woman with multiple sclerosis took citalopram 20 mg/day for 4 weeks and was found unconscious in her apartment (17). The main finding was a low plasma sodium (108 mmol/1). As a result of... 

A 20-year-old woman attended a rave , where she took ecstasy and drank large amounts of water (often suggested to prevent dehydration and other life-threatening consequences) (97). She felt drowsy and had a headache. After lying still for 3 hours, she had a tonic-clonic seizure and was brought to hospital, where her plasma sodium concentration was 112 mmol/1 and she had cerebral edema. She was treated with hypertonic saline and recovered fully. 

Hyponatremia occurs in approximately a third of patients in the first week or two after SAH and is related to the severity of the initial presentation. It is not usually caused by inappropriate antidiuretic hormone secretion but by salt wasting, in which there is excessive loss of salt and water by the kidneys with a decrease in plasma volume. Below a plasma sodium of approximately 125mmol/l, correction is necessary by plasma volume expansion (Berendes et al. 1997). 

Except for respiratory and dermal insensible water-vapor losses, all remaining water lost by the body contains electrolytes, mainly sodium and chloride. The normal cation and anion constituent composition of the fluid spaces is given in Table IV. In the extracellular fluid space, sodium is the major cation and chloride the major anion. Those two ions constitute 95 of the extracellular fluid osmolality. Changes in plasma sodium concentration reflect changes in extracellular fluid volume. Potassium is the major cellular cation and phosphates and proteins comprise the major anions. The total cellular osmolality (175 + 135 = 310 mosraol/kg H2O) is equal to the total extracellular osmolality (155 + 155 = 310 mosmol/kg HaO) therefore, equal total osmotic concentrations are maintained between two fluid compartments of widely different ionic contents (Table IV). 

Overdose is treated by use of i.v. fluid to maintain a good urine output guided by frequent measurement of plasma electrolytes and osmolality. Hyper-natraemia indicates probable diabetes insipidus and isotonic dextrose should then be used until plasma sodium concentration and osmolality become normal. Isotonic saline foriirs part of the fluid regimen (but overuse may result in hypematrae-mia) and potassium supplement will be required. Haemodialysis is effective but may have to be repeated frequently as plasma concentration rises after acute reduction (due to equilibration as lithium leaves cells and also by continued absorption from sustained-release formulahons). 

The most common chronic adverse effect is hyponatraemia, but this is usually mild, asymptomatic and of no clinical significance. Routine serum monitoring of the plasma sodium is indicated only where there is special risk, e.g. patients taking diuretics or the elderly. 

About 50% of patients with cirrhosis develop ascites within 10 years of diagnosis and 50% of these will die within 2 years. The process by which ascites forms in cirrhosis is not fully understood but appears to involve the accumulation of vasodilator substances, activation of the renin-angiotensin-aldosterone system (causing renal retention of sodium and water), and the production of antidiuretic hormone (causing hyponatraemia due to dilution, not deficiency, of plasma sodium). 

The aim is to induce natriuresis with consequent loss of water. Fluid restriction is unnecessary unless the plasma sodium falls below 120mmol/l. The initial management must include a diagnostic tap of the ascitic fluid as spontaneous bacterial peritonitis complicates up to 25% of patients on presentation. 

A variety of tumours, e.g. oat-cell limg cancer, can make vasopressin, and of course they are not subject to normal homeostatic mechanisms. SIADH also occurs in some CNS and respiratory disorders (infection). Dilutional hyponatraemia follows, i.e. low plasma sodium with an inappropriately low plasma osmolality and high urine osmolality. When the plasma sodium approaches 120 mmol/I treatment should be with fluid restriction (< 500 ml/day). Treatment is primarily of the imderlying disorder accompanied by fluid restriction. Chemotherapy to the causative tumour or infection is likely to be the most effective treatment. Demeclocycline, which inhibits the renal action of vasopressin, is useful Infusion of isotonic or hypertonic saline must be reserved for extreme emergencies, associated with stupor, and undertaken with great caution. Rapid correction of hyponatraemia must be avoided because of the risk of central pontine myelinolysis the rate of correction must not exceed 12 mmol/1 per 24 h. 

To simplify these calculations, the capital cost of the instrument may be amortized over 5 or 6 years and maintenance costs ignored. The average daily cost can then be calculated and will be the same whether the instrument is used or not. Reagent costs are simple to calculate and are usually small in relation to other costs. Examples of labor and equipment costs of 5 commercial flame photometers, used to measure plasma sodium and potassium simultaneously, were given by Broughton and Dawson (B18). With small numbers of analyses, the least expensive instrument was the cheapest to run, but despite wide differences in capital outlay and labor requirements, the cost per analysis for the 5 instruments... 

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