What inferences can be made regarding fluid volume deficits and serum sodium level

Hypernatremia is a serum sodium concentration > 145 mEq/L (> 145 mmol/L). It implies a deficit of total body water relative to total body sodium caused by water intake being less than water losses. A major symptom is thirst; other clinical manifestations are primarily neurologic (due to an osmotic shift of water out of brain cells), including confusion, neuromuscular excitability, seizures, and coma. Diagnosis requires measurement of serum sodium and sometimes other laboratory tests. Treatment is usually controlled water replacement. When the response to treatment is poor, testing (eg, monitored water deprivation or administration of vasopressin) is directed at detecting causes other than decreased water intake.

Hypernatremia reflects a deficit of total body water (TBW) relative to total body sodium content. Because total body sodium content is reflected by extracellular fluid (ECF) volume status, hypernatremia must be considered along with status of the ECF volume:

  • Hypovolemia

  • Euvolemia

  • Hypervolemia

Hypernatremia usually involves an impaired thirst mechanism or limited access to water, either as contributing factors or primary causes. The severity of the underlying disorder that results in an inability to drink in response to thirst and the effects of hyperosmolality on the brain are thought to be responsible for a high mortality rate in hospitalized adults with hypernatremia. There are several common causes of hypernatremia (see table Principal Causes of Hypernatremia Principal Causes of Hypernatremia

What inferences can be made regarding fluid volume deficits and serum sodium level
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What inferences can be made regarding fluid volume deficits and serum sodium level

Renal causes of hypernatremia and volume depletion include therapy with diuretics. Loop diuretics inhibit sodium reabsorption in the concentrating portion of the nephrons and can increase water clearance. Osmotic diuresis can also impair renal concentrating capacity because of a hypertonic substance present in the tubular lumen of the distal nephron. Glycerol, mannitol, and occasionally urea can cause osmotic diuresis resulting in hypernatremia.

Essential hypernatremia (primary hypodipsia) occasionally occurs in children with brain damage and in chronically ill older adults. It is characterized by an impaired thirst mechanism (eg, caused by lesions of the brain’s thirst center). Altered osmotic trigger for vasopressin release is another possible cause of euvolemic hypernatremia; some lesions cause both an impaired thirst mechanism and an altered osmotic trigger. The nonosmotic release of vasopressin appears intact, and these patients are generally euvolemic.

Hypernatremia is common among older adults, particularly postoperative patients and those receiving tube feedings or parenteral nutrition. Other contributing factors may include the following:

  • Dependence on others to obtain water

  • Impaired thirst mechanism

  • Impaired renal concentrating capacity (due to diuretics, impaired vasopressin release, or nephron loss accompanying aging or other renal disease)

  • Impaired angiotensin II production (which may contribute directly to the impaired thirst mechanism)

Symptoms and Signs of Hypernatremia

The major symptom of hypernatremia is thirst. The absence of thirst in conscious patients with hypernatremia suggests an impaired thirst mechanism. Patients with difficulty communicating or ambulating may be unable to express thirst or obtain access to water. Sometimes patients with difficulty communicating express thirst by becoming agitated.

The major signs of hypernatremia result from central nervous system (CNS) dysfunction due to brain cell shrinkage. Confusion, neuromuscular excitability, hyperreflexia, seizures, or coma may result. Cerebrovascular damage with subcortical or subarachnoid hemorrhage and venous thromboses have been described in children who died of severe hypernatremia.

In chronic hypernatremia, osmotically active substances are generated in CNS cells (idiogenic osmoles) and increase intracellular osmolality. Therefore, the degree of brain cell dehydration and resultant CNS symptoms are less severe in chronic than in acute hypernatremia.

When hypernatremia occurs with abnormal total body sodium, the typical symptoms of volume depletion Volume Depletion 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... read more or volume overload Volume Overload Volume overload generally refers to expansion of the extracellular fluid (ECF) volume. ECF volume expansion typically occurs in heart failure, kidney failure, nephrotic syndrome, and cirrhosis... read more are present. Patients with renal concentrating defects typically excrete a large volume of hypotonic urine. When losses are extrarenal, the route of water loss is often evident (eg, vomiting, diarrhea, excessive sweating), and the urinary sodium concentration is low.

  • Serum sodium

The diagnosis is by measuring serum sodium. Physical examination is done to determine if volume depletion or overload is also present. In patients who do not respond to simple rehydration or in whom hypernatremia recurs despite adequate access to water, further diagnostic testing is warranted. Determination of the underlying disorder requires assessment of urine volume and osmolality, particularly after water deprivation.

  • Replacement of intravascular volume and of free water

Replacement of both intravascular volume and free water is the main goal of treatment. Oral hydration is effective in conscious patients without significant gastrointestinal dysfunction. In severe hypernatremia or in patients unable to drink because of continued vomiting or mental status changes, IV hydration is preferred. Hypernatremia that has occurred within the last 24 hours should be corrected over the next 24 hours. However, hypernatremia that is chronic or of unknown duration should be corrected over 48 hours, and the serum osmolality should be lowered at a rate of no faster than 0.5 mOsm/L/hour to avoid cerebral edema caused by excess brain solute. The amount of water (in liters) necessary to replace existing deficits may be estimated by the following formula:

What inferences can be made regarding fluid volume deficits and serum sodium level

where TBW is in liters and is estimated by multiplying weight in kilograms by 0.6 for men and by 0.5 for women; serum sodium can be in mEq/L or mmol/L. This formula assumes constant total body sodium content. In patients with hypernatremia and depletion of total body sodium content (ie, patients who have volume depletion), the free water deficit is greater than that estimated by the formula.

In patients with hypernatremia and ECF volume overload (excess total body sodium content), the free water deficit can be replaced with 5% dextrose in water (D/W), which can be supplemented with a loop diuretic. However, too-rapid infusion of 5% D/W may cause glucosuria, thereby increasing salt-free water excretion and hypertonicity, especially in patients with diabetes mellitus. Other electrolytes, including serum potassium, should be monitored and should be replaced as needed.

In patients with hypernatremia and euvolemia, free water can be replaced using either 5% D/W or 0.45% saline.

In patients with hypernatremia and hypovolemia, particularly in patients with diabetes with nonketotic hyperglycemic coma, 0.45% saline can be given as an alternative to a combination of 0.9% normal saline and 5% D/W to replenish sodium and free water. Alternatively, ECF volume and free water can be replaced separately, using the formula given previously to estimate the free water deficit. When severe acidosis (pH < 7.10) is present, sodium bicarbonate solution can be added to 5% D/W or 0.45% saline, as long as the final solution remains hypotonic.

  • Hypernatremia is usually caused by limited access to water or an impaired thirst mechanism, and less commonly by diabetes insipidus.

  • Manifestations include confusion, neuromuscular excitability, hyperreflexia, seizures, and coma.

  • Patients who do not respond to simple rehydration or in whom there is no obvious cause may need assessment of urine volume and osmolality, particularly after water deprivation.

  • Replace intravascular volume and free water orally or intravenously at a rate dictated by how acutely (< 24 hour) or chronically (> 24 hour) the hypernatremia has developed, while watching other serum electrolyte levels (especially potassium and bicarbonate) as well.

Drug NameSelect Trade

vasopressin

Pitressin, Vasostrict

mannitol

Aridol, BRONCHITOL, Osmitrol , Resectisol

urea

Aluvea , BP-50% Urea , BP-K50, Carmol, CEM-Urea, Cerovel, DermacinRx Urea, Epimide-50, Gord Urea, Gordons Urea, Hydro 35 , Hydro 40, Kerafoam, Kerafoam 42, Keralac, Keralac Nailstik, Keratol, Keratol Plus, Kerol, Kerol AD, Kerol ZX, Latrix, Mectalyte, Nutraplus, RE Urea 40, RE Urea 50 , Rea Lo, Remeven, RE-U40, RYNODERM , U40, U-Kera, Ultra Mide 25, Ultralytic-2, Umecta, Umecta Nail Film, URALISS, Uramaxin , Uramaxin GT, Urea, Ureacin-10, Ureacin-20, Urealac , Ureaphil, Uredeb, URE-K , Uremez-40, Ure-Na, Uresol, Utopic, Vanamide, Xurea, X-VIATE

sodium bicarbonate

Alka-Seltzer Heartburn Relief, Baros, Neut

angiotensin ii

GIAPREZA

dextrose

Advocate Glucose SOS, BD Glucose, Dex4 Glucose, Glutol , Glutose 15 , Glutose 45 , Glutose 5

How does sodium affect fluid volume?

Gain of sodium leads to seeking and retaining water with expansion of the extracellular fluid volume. Loss of sodium, at least initially, leads to loss of water and contraction in the extracellular fluid volume. Thus, sodium metabolism governs the volume of the extracellular fluid.

What fluid shift would occur with a low serum sodium level?

HYPONATREMIA is a common fluid and electro- lyte disturbance. The decrease in plasma sodium concentration is usually associated with a reduction in body fluid osmolality, a state that causes shifts of water between the interstitium and the cells.

How does low sodium affect fluid balance?

It is very important for maintaining blood pressure. Sodium is also needed for nerves, muscles, and other body tissues to work properly. When the amount of sodium in fluids outside cells drops below normal, water moves into the cells to balance the levels. This causes the cells to swell with too much water.

How does dehydration affect sodium levels?

Chronic, severe vomiting or diarrhea and other causes of dehydration. This causes your body to lose electrolytes, such as sodium, and also increases ADH levels. Drinking too much water. Drinking excessive amounts of water can cause low sodium by overwhelming the kidneys' ability to excrete water.