Volume Depletion

ByJames L. Lewis III, MD, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham
Reviewed/Revised Apr 2022
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Volume depletion, or extracellular fluid (ECF) volume contraction, occurs as a result of loss of total body sodium. Causes include vomiting, excessive sweating, diarrhea, burns, diuretic use, and kidney failure. Clinical features include diminished skin turgor, dry mucous membranes, tachycardia, and orthostatic hypotension. Diagnosis is clinical. Treatment involves administration of sodium and water.

(See also Water and Sodium Balance and Overview of Disorders of Fluid Volume.)

Because water crosses plasma membranes in the body via passive osmosis, loss of the major extracellular cation (sodium) quickly results in water loss from the extracellular fluid (ECF) as well as from intracellular (ICF) spaces. In this way, sodium loss always causes water loss. However, depending on many factors, serum sodium concentration can be high, low, or normal in volume-depleted patients (despite the decreased total body sodium content).

Total body sodium content and ECF volume are related to effective circulating volume. A large enough decrease in ECF causes a decrease in effective circulating volume, which in turn causes decreased organ perfusion and leads to clinical sequelae. Common causes of volume depletion are listed in the table Common Causes of Volume Depletion.

Table

Symptoms and Signs of Volume Depletion

When fluid loss is < 5% of ECF volume (mild volume depletion), the only sign may be diminished skin turgor (best assessed at the upper torso); note that skin turgor may be low in older patients regardless of volume status. Patients may complain of thirst. Dry mucous membranes do not always correlate with volume depletion, especially in older patients and in mouth-breathers. Oliguria is typical.

When ECF volume has diminished by 5 to 10% (moderate volume depletion), orthostatic tachycardia, hypotension, or both are usually, but not always, present. Also, orthostatic changes can occur in patients without ECF volume depletion, particularly patients deconditioned or bedridden. Skin turgor may decrease further.

When fluid loss is > 10% of ECF volume (severe volume depletion), signs of shock (eg, tachypnea, tachycardia, hypotension, confusion, poor capillary refill) can occur.

Diagnosis of Volume Depletion

  • Clinical findings

  • Rarely plasma osmolality and urine chemistries

Volume depletion is suspected in patients at risk, most often in patients with a history of inadequate fluid intake (especially in comatose or disoriented patients), increased fluid losses, diuretic therapy, and renal or adrenal disorders.

Diagnosis is usually clinical. If accurate patient weights immediately before and after fluid loss are known, the difference is an accurate estimate of volume loss; for example, pre- and post-workout weights are sometimes used to monitor dehydration in athletes.

When the cause is obvious and easily correctable (eg, acute gastroenteritis in otherwise healthy patients), laboratory testing is unnecessary; otherwise, serum electrolytes, BUN, and creatinine are measured. Plasma osmolality and urine sodium, creatinine, and osmolality are measured when there is suspicion of clinically meaningful electrolyte abnormality that is not clear from results of serum tests and for patients with cardiac or renal disease. When metabolic alkalosis is present, urine chloride is also measured.

Some devices can help assess volume status but are not in widespread use. Point-of-care ultrasonography evaluating inferior vena cava distension is sometimes used to assess volume status when the severity of volume loss is unclear. Also, ultrasonography of the lungs can show findings of pulmonary edema and thus fluid overload. Central venous pressure and pulmonary artery occlusion pressure are decreased in volume depletion, but measurement with an invasive device such as a central venous catheter or pulmonary artery catheter is rarely required, although it is occasionally necessary for patients for whom even small amounts of added volume may be detrimental, such as those with unstable heart failure or advanced chronic kidney disease.

The following concepts are helpful when interpreting urine electrolyte and osmolality values:

  • During volume depletion, normally functioning kidneys conserve sodium. Thus, the urine sodium concentration is usually low,< 15 mEq/L (< 15 mmol/L); the fractional excretion of sodium (urine sodium/serum sodium divided by urine creatinine/serum creatinine) is usually < 1%; also, urine osmolality is often high,> 450 mOsm/kg (> 450 mmol/kg).

  • When metabolic alkalosis is combined with volume depletion, urine sodium concentration may be high because large amounts of bicarbonate are spilled in the urine, obligating the excretion of sodium to maintain electrical neutrality. In this instance, a urine chloride concentration of < 10 mEq/L (< 10 mmol/L) more reliably indicates volume depletion.

  • Misleadingly high urinary sodium (generally > 20 mEq/L [> 20 mmol/L]) or low urine osmolality can also occur due to renal sodium losses resulting from renal disease, diuretics, or adrenal insufficiency.

Volume depletion frequently increases the BUN and serum creatinine concentrations; the ratio of BUN to creatinine is often > 20:1. Values such as hematocrit often increase in volume depletion but are difficult to interpret unless baseline values are known.

Clinical Calculators

Treatment of Volume Depletion

  • Replacement of sodium and water

The cause of volume depletion is corrected and fluids are given to replace existing volume deficits as well as any ongoing fluid losses and to provide daily fluid requirements.

Mild-to-moderate volume deficits may be replaced by increased oral intake of sodium and water when patients are conscious and not vomiting; oral rehydration regimens in children are discussed elsewhere. Tube feedings can also be used if oral intake is limited or not safe for some reason.

When volume deficits are severe or when oral fluid replacement is impractical, IV 0.9% saline or a buffered electrolyte solution (eg, Ringer's lactate) is given. Both are well tolerated and safe, but Ringer’s lactate and other buffered solutions have lower chloride concentrations and may reduce development of hyperchloremic metabolic acidosis. Recent evidence seems to favor use of Ringer's lactate over saline, but the issue is not settled. Because both of these solutions distribute evenly into the extracellular space, three to four times the deficit in intravascular volume needs to be given. Typical IV regimens are given elsewhere.

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