Sodium loss from sweating

Q2 Sweat is a hypotonic solution containing water, sodium and chloride. Loss of sweat decreases ECF volume and increases its osmolarity. If the volume lost is not great, the kidney can compensate by retaining extra sodium and water from the glomerular filtrate. But when loss of fluid via sweat is severe, the compensatory mechanisms may cause the kidney to stop producing urine for a time (anuria). 

Additionally, lithium excretion is directly related, in an inverse way, to sodium excretion. Conditions leading to excess sodium elimination will cause a corresponding increase in the amount of lithium retained in the body. Excessive sodium loss occurs from diarrhea, vomiting, fever, dehydration, profuse sweating, diuretic medications, and severely salt-restricted diets. 

The most common cause of hyponatremia in hospital patients is SIADH. However, other disorders can cause dilutional hyponatremia and must be differentiated from SIADH. These conditions include (1) congestive heart failure, (2) renal insufficiency, (3) nephrotic syndrome, (4) liver cirrhosis, and (5) hypothyroidism. Excessive administration of hypotonic fluids and treatment with drugs that stimulate AVP (e.g., chlorpropamide, vincristine, clofibrate, carbamazepine, nicotine, phenothiazines, and cyclophosphamide) can cause dilutional hyponatremia as well. Hyponatremia may also occur from renal or extrarenal sodium losses (depietional hyponatremia) as a result of vomiting, diarrhea, excessive sweating, diuretic abuse, saltlosing nephropathy, or mineralocorticoid deficiency. 

Sodium losses are just as variable. In practical terms, urinary sodium excretion matches sodium intake. Most sodium excretion is via the kidneys. Some sodium is lost in sweat (approximately 5 mmol/ day) and in the faeces (approximately 5 mmol/day). In disease the gastrointestinal tract is often the major route of sodium loss. This is a very important clinical point, especially in paediatric practice, as infantile diarrhoea may result in death from salt and water depletion. 

It is noteworthy that certain vegetarians may consume only small amounts of sodium because their diets are based mainly upon unprocessed, unsalted plant foods which contain only traces of the mineral. Animal foods and commercially processed plant foods usually contain sufficient sodium so that the adding of extra salt is not necessary. However, normally healthy people on low intakes of salt may suffer from sodium deficiency if they are exposed to hot environments, or if they engage in strenuous activities that provoke heavy losses of sweat. 

Replacement of water and electrolyte losses incurred during exercise is an important part of the recovery process in the postexercise period. This requires ingestion of fluid in excess of the volume of sweat lost to allow for ongoing water losses from the body. Re-establishment of water balance requires replacement of solute, especially sodium, losses as well as volume replacement. If food containing electrolytes is not consumed at this time, electrolytes, especially sodium, must be added to drinks to prevent diuresis and loss of the ingested fluid. 

Abnormally high concentrations of sodium and chloride are found in sweat due to impaired reabsorption within the sweat duct from loss of CFTR channels. Patients are usually asymptomatic (other than a characteristic salty taste to the skin).2 In rare instances such as hot weather or excessive sweating during physical activity, patients may become dehydrated and experience symptoms of hyponatremia (nausea, headache, lethargy, and confusion). Similar CFTR defects are also seen in the salivary glands, manifested by increased saliva viscosity and impaired salivary function. 

A sweat rate of one liter per hour, as occurs with continuous moderate exercise, would lead to the loss of about 40 mmol of Na per hour. A 5-hour running marathon would result in the loss of 200 mmol of sodium. This loss represents depletion of about 12% of the sodium in the ECF. This loss does not, however, result in a drop in plasma sodium concentrations. Plasma sodium is maintained during prolonged exercise by the loss of plasma water, resulting in a drop in plasma volume. Experiments involving human subjects exercising on a stationary bicycle for 3 hours in a warm humid room suggested that about 10% of the water lost in sweat comes from plasma, 38% from interstitial fluid, and about 52% from intracellular fluids (Table 10.9). 

Hypernatremia, that is, sodium levels of 146 mEq/L (146 mmol/L) or higher, results from excessive sodium intake or sodium retention with excessive loss of water owing to diarrhea, diurehc medicahon use, vomiting, sweating, heavy respirahon, or severe bums. Therefore, these pahents are at highest risk and should be monitored closely. Elderly hospitalized pahents should be watched most carefully because many have chronic diseases that may be fatal in combinahon with excessive sodium and fluid loss. 

The nutritional requirement is a reflection of obligatory losses (maintenance) and the needs of growth, pregnancy, and lactation. Abnormal losses owing to disease, or in animals such as humans and horses which sweat extensively, raise the requirement. The impact of equine sweating is different from that in humans. Human sweat always contains sodium at concentrations well below plasma levels (and when aldosterone secretion is raised, levels of sweat sodium fall very low) horse sweat is hypertonic but this helps to offset the osmotic effect of the increased respiratory water loss during exertion, i.e., it may be a defense against hypernatremia, rather than a potential cause of sodium depletion. Similarly hypernatremia in many species induces dehydration natriuresis - an appropriate defense. 

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