Hypotonic fluids

If serum sodium rises more than 150 mEq/L or when euv-olemic, switch to hypotonic fluid replacement. Lactated Ringer s solution may prolong ketoacid production by promoting alkalinization... 

TBW depletion (often referred to as dehydration ) is typically a more gradual, chronic problem compared to ECF depletion. Because TBW depletion represents a loss of hypotonic fluid (proportionally more water is lost than sodium) from all body compartments, a primary disturbance of osmolality is usually seen. The signs and symptoms of TBW depletion include CNS disturbances (mental status changes, seizures, and coma), excessive thirst, dry mucous membranes, decreased skin turgor, elevated serum sodium, increased plasma osmolality, concentrated urine, and acute weight loss. Common causes of TBW depletion include insufficient oral intake, excessive insensible losses, diabetes insipidus, excessive osmotic diuresis, and impaired renal concentrating mechanisms. Long-term care residents are frequently admitted to the acute care hospital with TBW depletion secondary to lack of adequate oral intake, often with concurrent excessive insensible losses. 

Half-normal saline is a hypotonic fluid that provides free water in relative excess when compared to the sodium concentration. This crystalloid is typically used to treat patients... 

Hypernatremia is a serum sodium concentration greater than 145 mEq/L (145 mmol/L) and can occur in the absence of a sodium deficit (pure water loss) or in its presence (hypotonic fluid loss).19 The signs and symptoms of hypernatremia are the same as those found in TBW depletion. Symptoms of hypernatremia are evident with a serum concentration greater than 160 mEq/L (160 mmol/L) and usually consist of thirst, mental slowing, and dry mucous membranes. Signs and symptoms become more profound as hypernatremia worsens, with the patient demonstrating confusion, hallucinations, acute weight... 

Hypernatremia can result from water loss (e.g., diabetes insipidus [DI]) hypotonic fluid loss or, less commonly, hypertonic fluid administration or sodium ingestion. 

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). 

Loop diuretics can cause hjrpematremia by increasing free water clearance (net water loss in the form of hypotonic fluid) (99). Over-rapid correction should be avoided. 

Risk factors for this adverse effect are pre-existing renal disease, age over 65 years, dehydration, diabetes mellitus, hypertension, and a high infusion rate (SEDA-22, 345) (10,13,32,43,86,92). To minimize the risk of renal insufficiency, it has been suggested that immunoglobulin should be diluted with hypotonic fluid, that the infusion rate should be reduced, and that dosing intervals should be increased (89). Patients should be adequately hydrated and potent diuretics should be avoided (10). 

Crystalloid fluids rapidly pass from the circulation to the interstitial fluid. This means that their resuscitation effect may be short lived and they can cause edema. Only 30% of isotonic fluids and 10% of hypotonic fluids remain in the circulation after 30 min (Spalding Goodwin 1999). The increase in interstitial fluid may actually decrease tissue oxygen uptake in normal animals by increasing the diffusion distance between... 

It is possible to treat moderately dehydrated horses effectively with oral replacement solutions (ORSs) (McGinness et al 1996). Oral fluids do not need to be sterUe and can be made up on the farm they are, therefore, considerably cheaper and easier to transport than i.v. fluids. It is apparently not necessary to add glucose to oral fluids for horses (Sosa Leon et al 1995) but, if feasible, electrolytes should be added. Isotonic or hypotonic fluids should be adnunistered (Sosa Leon et al 1995). A possible isotonic solution consists of 4.9 g/1 table salt and... 

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. 

This includes patients with fluid losses caused by diarrhea, excessive sweating, and diuretics. This transient hypernatremic hyperosmolality results in osmotic release of ADH and stimulation of thirst. If sodium and water losses continue, more ADH is released as a result of hypovolemia. Patients who then drink water or who are given hypotonic fluids intravenously retain water and develop hyponatremia. Urine osmolality is generally greater than 450 mOsm/kg, reflecting the presence of ADH and formation of a concentrated urine. The urine sodium concentration is <20 mEq/L when sodium losses are extrarenal, as in patients with diarrhea, and >20 mEq/L in patients with renal sodium losses, as occurs in the setting of diuretic use or adrenal insufflciency. °... 

Patients with a contracted ECF volume and a low urine output include those who have sustained insensible water losses that exceed intake, as well as those with extrarenal losses of hypotonic fluids. On physical exam, one should search for postural hypotension, diminished skin turgor, and delayed capillary refill. The daily urine output is typically less than 1 L. 

Hypernatremia in patients nndergoing a postobstructive diuresis should be treated with infusion of hypotonic fluids such as 0.45% saline at maintenance rates of approximately 1.5 mL/kg per hour. It is important to avoid the temptation to administer fluids to replace urine output on a 1 mL 1 mL volume basis, because this tends to perpetuate the diuresis. 

The serum sodium concentration and fluid status should be monitored every 2 to 3 hours over the first 24 hours of admission in patients with symptomatic hypernatremia to permit appropriate adjustment in the rate of infusion of hypotonic fluids. After symptoms resolve and the serum sodium is less than 148 mEq/L, serum sodium determinations every 6 to 12 hours and fluid status assessment every 8 to 24 hours are generally sufficient to follow the course of therapy. 

Hypotonic fluids have a lower concentration of solutes (hypo-osmolality) than is found inside the cells, which causes fluid to flow into cells and out of the extracellular spaces. This causes cells to swell and possibly burst. 

Verify the fluids being given and avoid large volumes of hypotonic fluids. 

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