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Water and sodium
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
The diagnosis of SIADH is usually made by finding a urinary sodium concentration more than 20 mmol/L in the presence of euvolaemic hyponatraemia or low plasma osmolality and in the absence of hypovolaemia, oedema, impaired renal function, diuretic usage, adrenal insufficiency or hypothyroidism. According to the Bartter and Schwartz criteria for SIADH, the urinary osmolality is inappropriately concentrated in relation to the plasma osmolality, that is, in the hypoosmolar state the urine is not maximally diluted. In SIADH, the GFR is usually high, and plasma urea and urate concentrations tend to be low: During the intravenous administration of the posterior pituitary hormone oxytocin (Syntocinon) to induce labour (see Chapter 7). Oxytocin has an antidiuretic effect similar to that of the chemically closely related ADH. If 5 per cent dextrose saline is used as a carrier, the glucose is metabolized and the net effect is retention of solute-free water. Death from acute hypo-osmolality has resulted after prolonged infusion; oxytocin should be given in the smallest possible volume of isotonic saline, and the fluid balance and plasma sodium concentrations should be monitored carefully.Excess water intake can also occur if water intake exceeds water clearance (about 20 L/day), for example in beer potomania (excess beer intake) or psychogenic polydipsia.TURP (transurethral resection of the prostate) syndrome: water intoxication caused by an overload of hypotonic irrigation fluid (such as glycine) absorption from the open prostatic sinusoids during the procedure.
Acid-Base, Electrolyte And Renal Emergencies
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Causes include: Factitious ‘pseudohyponatraemia’associated with hyperglycaemia, hyperlipidaemia, hyperproteinaemiacorrect the sodium for hyperglycaemia by adjusting the serum sodium up by 1 mmol/L for every 3 mmol/L elevation in blood sugar.Hypovolaemic hyponatraemiaurinary sodium >20 mmol/L: renal causes including diuretics, Addison's disease, salt-losing nephropathy, glycosuria, ketonuriaurinary sodium <20 mmol/L: extrarenal losses such as vomiting, diarrhoea, burns, pancreatitis.Normovolaemic hyponatraemiaurine osmolality > serum osmolality: syndrome of inappropriate antidiuretic hormone secretion (SIADH) due to head injury, meningoencephalitis, CVA, pneumonia, COPD, neoplasia, human immunodeficiency virus (HIV) infection, drugs such as carbamazepine, NSAIDs and antidepressants such as SSRIspositive-pressure ventilation, porphyriaurine osmolality < serum osmolality: hypotonic post-operative fluids such as 5% dextrose or 4% dextrose 1/5 normal saline, transurethral resection of the prostate (TURP) irrigation fluid, psychogenic polydipsia, ‘tea and toast’ diet, beer potomania.Hypervolaemic hyponatraemiaurinary sodium <20 mmol/L: congestive cardiac failure, cirrhosis, nephrotic syndrome, hypoalbuminaemia, hepatorenal syndromeurinary sodium >20 mmol/L: steroids, cerebral salt wasting, chronic renal failure, hypothyroidism.
Approach to and management of abnormalities in plasma sodium
Published in Acta Clinica Belgica, 2019
If the daily solute excretion is for example 800 mOsm and the patient can dilute his urine to about 50–100 mOsm/kg H2O, he should be able to eliminate 8–16 l of urine daily, or 333–666 ml/h. These patients could sometimes drink very large volumes of water in a few hours, and overcome the quantitative diluting ability of their kidneys. Many of these patients may have some degree of impairment of the diluting ability, which may be of various origins (nicotine, psychotropic drugs, nausea associated with massive water intake, psychosis itself, enhanced sensitivity to ADH, reset osmostat). These patients frequently present with acute symptomatic hyponatremia (see later). In beer potomania, these patients frequently also stop eating, the only caloric intakes being represented by beer which contains very little protein and electrolytes. Low solute intake will increase the risk of hyponatremia (tea and toast hyponatremia) [3]. These patients (usually presenting a FE.Osm < 1%) if they don’t want to restrict their water intake are easily treated with a small increase in their daily osmole intake (like 15 g urea, representing 250 mmol).