Originally posted May 2005
By Sonia M. Astle, RN, MS, CCRN
Sonia Astle is a critical care clinical specialist at Inova Fairfax Hospital in Falls Church, VA, and a member of the RN editorial board. The author has no financial relationships to disclose.
A shift up. A shift down. Either way, an imbalance in electrolytes spells trouble for your patients. Averting a crisis hinges on your clinical skills. This review will help you sharpen them.
Electrolytes, or ions, are the charged particles in body fluids that help transmit electrical impulses for proper nerve, heart, and muscle function.1,2 The number of positive ions, called cations, and negative ions, called anions, is supposed to be equal. Anything that upsets this balance can have life-threatening consequences.
There's a long list of conditions that lead to electrolyte imbalances, including dehydration, diabetic ketoacidosis, cancer, and even head injury. But renal disease is at the top of the list.1-3 It's the kidneys' job to control fluid, electrolyte, and acid-base balance.
Because too much or too little of any one of the electrolytes quickly becomes a major problem of its own, doing everything possible to maintain the proper balance is a vital component of patient care. Therefore, monitoring electrolytes and checking for signs of an imbalance should be an integral part of your nursing assessment.
Here, then, is a review of the role each electrolyte plays, the causes of imbalances, and the corrective measures required.
Understanding sodium's effect on water balance
Sodium (Na), the most abundant cation in extracellular fluid, plays a key role in transmitting nerve impulses. It also helps maintain serum concentration, or osmolality.1
Water follows salt in the body, so a gain or loss in sodium results in a gain or loss in water. For instance, when you eat too much salt, the rise in serum osmolality triggers thirst and the release of antidiuretic hormone (ADH) from the pituitary gland. Thirst leads you to drink, while ADH signals the kidneys to hang onto water.1,2
The opposite is also true: Low serum osmolality from too little salt stops thirst and inhibits ADH release, allowing more water to be excreted by the kidneys.2
Hypernatremia occurs when either too much water is lost or too much salt is taken in. (You'll find a list of normal values and causes of electrolyte imbalances in the box on page 37). The elderly are particularly at risk for hypernatremia following surgery or a fever because of volume depletion, and because of a diminished thirst mechanism.4 All patients on fluid restrictions and those receiving diuretic therapy, hypertonic IV solutions, or tube feedings are at risk, as well.1,4 So, too, are patients with diabetes, because of dehydration related to their hyperglycemia.3
Regardless of the cause, patients with hypernatremia may appear thirsty, tachycardic, and lethargic.1,2 As their cells become more dehydrated, patients may develop disorientation, weakness, irritability, and muscle twitching. Urine output is generally low as the body tries to compensate by hanging onto water. The exception is untreated diabetes insipidus, where a lack of ADH results in a high urine output—possibly as much as 20 liters in 24 hours.1,2 Regardless, though, of whether urine output is high or low, seizures, coma, or death may result if hypernatremia is left untreated.1,2
Correcting the situation requires that you focus on the underlying cause. That may be as simple as replacing volume orally or by the IV administration of isotonic solutions such as normal saline.5 Or it may be as complex as putting the patient on dialysis. Part of your routine nursing care for the hypernatremic patient will involve monitoring serum sodium and osmolality and administering fluids based on the results.5 You'll also carefully monitor intake and output, and avoid overhydration.
The flip side of the sodium equation is hyponatremia, which usually occurs when the body loses more sodium than water or when excess water dilutes the normal sodium concentration.1,2 Dilutional hyponatremia can be caused by excess fluid intake, and conditions such as congestive heart failure or syndrome of inappropriate antidiuretic hormone secretion (SIADH).2
The neurological symptoms of hyponatremia are similar to those of hypernatremia—lethargy and confusion—with the possible addition of nausea and vomiting resulting from cerebral edema.2 Other signs and symptoms depend upon the cause. Patients who've lost sodium through diarrhea, certain diuretics, suctioning, or laxatives, for example, may show signs of dehydration, including tachycardia and hypotension. Those with dilutional hyponatremia may show signs of fluid overload, such as hypertension and difficulty breathing.
Treatment depends upon both the degree of sodium deficiency and the cause. In cases of mild hyponatremia, an increased intake of dietary sodium may be ordered, while patients who are both hyponatremic and hypovolemic may receive IV fluid replacement using solutions containing normal saline.6 Those with mild dilutional hyponatremia from overadministration of free water may need nothing more than the restriction of fluid intake. This approach is also appropriate for patients with hyponatremia caused by SIADH.2,5,6
Severe hyponatremia, however, is a medical emergency: Permanent neurological damage can occur when serum sodium falls below 110 mEq/L.2 Giving hypertonic saline (3% NaCl) solution is the treatment of choice, but must be done with caution: A rapid increase in serum sodium can cause fluid overload and cardiac failure, as well as cerebral osmotic demyelination syndrome—a condition caused by osmotic injury to myelinated nerve fibers that leads to paralysis and death.2,5
Other imbalances to watch for
Potassium (K), magnesium (Mg), calcium (Ca), and phosphorus (PO4) imbalances can also alter the electrical equilibrium of the cells. The end result? Serious changes in cardiac conduction that can quickly turn lethal.1,2 Let's look at each of these electrolytes and the implications that an imbalance will have on your care.
Potassium. This electrolyte is the major intracellular cation. The 2% that's found in extracellular fluid is crucial to neuromuscular and cardiac function.2 Normally, elevated serum potassium stimulates the release of aldosterone, a hormone produced by the adrenal gland. In the kidneys, aldosterone triggers the excretion of potassium and the retention of sodium until serum potassium levels return to normal.2
But when the kidneys aren't functioning properly, that correction doesn't take place. Not surprisingly, renal disease is the most common cause of hyperkalemia, but acidosis, aldosterone deficiency, sodium depletion, and excess oral intake of potassium supplements are among a number of other possible causes. Signs and symptoms of hyperkalemia include abdominal cramping, fatigue, lethargy, and muscle weakness or paralysis.
Severe hyperkalemia will slow cardiac impulse conduction, producing classic changes on EKG:1,2 Tall, peaked T waves are often seen first, followed by a prolonged PR interval and widened QRS complex, signifying delayed conduction, and a shortened QT interval. Left untreated, the excess potassium will continue to suppress conduction until cardiac arrest occurs.1
Severe hyperkalemia requires rapid action: Stop any potassium administration, and give IV calcium chloride or calcium gluconate, as ordered, to stimulate conduction.5 The doctor may also order IV sodium bicarbonate, insulin and 50% dextrose, or albuterol to try to shift potassium out of the bloodstream and back into the cells.5
Depending upon their kidney function, patients with hyperkalemia that is not severe may be given IV diuretics to promote potassium excretion by the kidneys or a resin such as sodium polystyrene sulfonate (Kayexalate) that will bind potassium in the gut. But if these efforts fail, hemodialysis may be required in addition to treating the underlying cause.2,5
When it comes to hypokalemia, diuretic therapy with inadequate potassium replacement is the most common cause, but patients who lose large amounts of potassium through nasogastric suctioning and diarrhea, for instance, are also at risk.1,2 Interestingly, so, too, are patients who were recently hyperkalemic—especially when acidosis is the cause or they're given too much of a drug that brings the potassium down. In acidosis, as pH returns to normal, potassium returns to the cells, lowering serum potassium and increasing the risk of hypokalemia.1,2
Symptoms of hypokalemia include muscle weakness or tenderness, leg cramps, drowsiness, confusion, loss of appetite, abdominal distention, and abnormal cardiac conduction.
Look for flattened or inverted T waves and a depressed ST segment on an EKG tracing. The lack of potassium makes cardiac muscle irritable, increasing the risk of premature atrial and/or ventricular contractions that can trigger ventricular tachycardia, which can progress to fibrillation and death.2
Initial treatment of hypokalemia, especially when it is accompanied by cardiac symptoms, focuses on replacing potassium.2,5 But this requires great care: Given too rapidly, IV potassium can cause cardiac arrest, so never administer it by IV push.5 Follow your institution's protocol, using a pump, if possible, to regulate the infusion so that it runs in over at least an hour when 15 - 20 mEqs are mixed in 100 mls of solution.
Because potassium is very irritating to tissues, administration through a central line is recommended.5 For the same reason, you should give oral preparations with food to reduce gastric irritation and abdominal discomfort. Report continued complaints of abdominal pain or distention to the physician. This could be a sign of upper GI ulcers caused by potassium.1,4
Magnesium. This cation is found primarily in the cells and is responsible for reactions that involve muscle function, energy production, and carbohydrate and protein metabolism.7 Renal failure is the major cause of hypermagnesemia.1,7 Other causes include excessive intake of magnesium-containing antacids and laxatives and conditions that produce acidosis such as diabetic ketoacidosis.3
Signs of hypermagnesemia include lethargy, altered mental status that can progress to coma, respiratory depression, and muscle weakness. Impaired cardiac conduction and contractility produce bradycardia and hypotension and can progress to a full cardiac arrest.1,3,7 EKG changes include a prolonged PR interval, widened QRS complex, and lengthened QT interval.7
If a patient's renal function is normal, treatment may include diuretics to promote magnesium loss. Calcium gluconate given intravenously can help counteract muscle weakness and improve cardiac function.5,7 Patients with severe hypermagnesemia and renal failure may need hemodialysis.
The other side of the magnesium equation is hypomagnesemia. It's common in critically ill patients and is associated with high mortality rates.7 Diuretic therapy, chronic alcoholism, cirrhosis, pancreatitis, and preeclampsia can all cause excessive magnesium loss, as can losses from the GI tract through nasogastric suctioning, fistula drainage, and diarrhea.
Signs and symptoms of hypomagnesemia include muscle weakness or tremors, anorexia, nausea, and dizziness, as well as neurologic changes including lethargy, confusion, and coma.7 Like hypokalemia, hypomagnesemia increases cardiac muscle irritability and the potential for ventricular dysrhythmias, especially in patients with a recent MI.2
EKG changes associated with low serum magnesium are similar to those seen in hypokalemia: a flat or inverted T wave and ST segment depression. There is also a shortened QT interval.7
Treatment focuses on giving the patient magnesium—either in IV or oral form—as ordered to return levels to normal.5,7 This is especially important in patients recovering from an acute MI. Research has shown that maintaining adequate serum magnesium levels in these patients can significantly improve ventricular function and reduce mortality rates.7
Calcium and phosphorus. These two electrolytes are inversely related in the blood: When calcium levels are high, phosphorus levels are low, and vice versa.1,2
Calcium is a cation with multiple functions, including transmitting nerve impulses, maintaining cell wall permeability, and activating the body's clotting mechanism.1 It's also involved in contracting cardiac and smooth muscle, generating cardiac impulses, mediating cardiac pacemaker function, and forming bones and teeth.
Phosphorus, the major intracellular anion, also plays a major role in bone formation.1 It's necessary for energy production in the cells and for carbohydrate, protein, and fat metabolism, as well.1,2 Phosphorous also helps maintain acid-base balance by buffering hydrogen ions.1,2
Parathyroid hormone (PTH) is responsible for regulating calcium and phosphorus. When calcium levels are low, PTH increases calcium reabsorption, and blocks phosphorus from being reabsorbed.
Hypocalcemia can result from diarrhea, diuretics, or acute pancreatitis. It can also be caused by malignancies that steal calcium for abnormal bone formation, conditions that affect the parathyroid gland and thus interfere with PTH production, and disorders that interfere with the availability of calcitrol, such as vitamin D deficiency and malabsorption syndromes.1,2
The drop in calcium that occurs in the presence of these disorders triggers a concomitant rise in phosphorus. But there are primary triggers for hyperphosphatemia to watch for, as well. Hyperphosphatemia can occur in patients with normal renal function if they abuse laxatives that are high in phosphorus or have too much of the mineral in their diet.
Both hypocalcemia and hyperphosphatemia can cause lethargy, fatigue, bone or joint pain, and sudden seizures. Low calcium levels also produce neuromuscular symptoms, including tremors, cramps, and numbness or tingling in the extremities and around the mouth. Patients may also complain of nausea, abdominal distention, vomiting, or constipation and develop cardiac symptoms, including life-threatening ventricular dysrhythmias.
EKG tracings will show prolonged ST segments and QT intervals.1,2 Decreased cardiac output and vascular smooth muscle relaxation produce decreases in BP that can progress to circulatory collapse.
Treatment focuses on increasing calcium and lowering phosphorus.5 Give IV calcium gluconate or calcium chloride or oral preparations, as ordered. Aluminum hydroxide gels that bind to phosphorus are given to increase elimination through the bowel.5 Patients with normal renal function may also receive the diuretic acetazolamide (Diamox) to promote renal excretion of phosphorus.2,5 When necessary, hemodialysis is used to quickly correct hyperphosphatemia.
Now let's take a look at the clinical picture for hypercalemia and hypophosphatemia. Causes of hypercalcemia include excessive use of dietary supplements containing calcium and vitamin D, which increase calcium reabsorption, and hyperparathyroidism. A primary cause of low serum phosphorus is chronic alcoholism.
Symptoms of hypercalcemia and hypophosphatemia include lethargy, fatigue, changes in mental status, anorexia, nausea, diminished bowel sounds, and constipation. Patients may also complain of bone pain; flank and thigh pain is associated with stones formed by excess calcium in the kidneys. Cardiovascular effects include hypertension and conduction abnormalities, seen as AV blocks on EKG, that can progress to cardiac arrest.1,2
IV saline infusions and diuretics are given to lower serum calcium through increased renal excretion.2,5 Steroids may also be administered to decrease intestinal reabsorption of calcium and mithramycin (Mithracin) is given to stimulate calcium deposits in bones.5 Phosphorus replacements can be given orally or by IV infusion.
Acid-base balance must be maintained
Chloride (Cl) and bicarbonate (HCO3) are the major extracellular anions. While both play an important role in maintaining acid-base balance, bicarbonate is by far the star of the show.1,2 Bicarbonate is the body's major buffer system. It helps keep the ratio between acids and bases in a tight range that's numerically expressed as the pH (normal pH is 7.35 - 7.45).1 A rise in pH above normal (alkalosis) or below normal (acidosis) causes cellular damage and can eventually lead to a patient's death.
For its part, chloride exists in an inverse relationship with bicarbonate.1 When there's too little chloride, bicarbonate builds up, and metabolic alkalosis results. The flip side of this—too much chloride—is a bit more complicated. If chloride is high and sodium is normal, the patient may be acidotic.1,2 If chloride is high and the sodium is also high, the patient is likely to be dehydrated.
One way to determine the cause of an acid-base imbalance is by calculating the anion gap.2,5 To calculate this gap, you need to take your patient's lab results and add the chloride and bicarbonate values. Then, subtract the sum of the two from the value for sodium. The normal anion gap range is 8 - 12.5
A high anion gap (>12) is indicative of conditions such as diabetic- or alcohol-induced ketoacidosis.5 A high anion gap may also be your first indication of lactic acidosis in patients with shock or sepsis. A normal anion gap with elevated chloride levels should also raise a flag for acidosis. That's because in cases of diarrhea and renal tubular acidosis, bicarbonate is lost, and chloride is retained to maintain electrical neutrality.1 Either way, interventions focus on treating the underlying cause of the acidosis.5
A low anion gap indicates alkalosis and hypochloremia from vomiting, nasogastric suctioning, or diuretic therapy.2,5 But other causes of alkalosis include Cushing's syndrome, excessive aldosterone secretion, and hypokalemia. Massive blood transfusions, over-administration of IV fluids containing bicarbonate, and excessive intake of antacids containing sodium bicarbonate can also cause bicarbonate levels to rise.
Again, treatment focuses on resolving the underlying cause. Patients with alkalosis may receive acetazolamide.5 The drug lowers bicarbonate levels by increasing its excretion in the urine and prevents the formation of new bicarbonate.2,5 Prolonged use can lead to acidosis, however, so watch bicarbonate levels closely.5
Your careful attention to bicarbonate, chloride, and the other electrolytes mentioned here, can have a tremendous impact on your patient's well-being. Understanding what the lab values mean in relation to changes in a patient's condition can be a challenge. But getting a firm handle on things will ensure that you take the necessary steps to correct imbalances before the situation becomes dire.
REFERENCES
1. Kee, J., Paulanka, B., & Purnell, L. (2004). Fluids and electrolytes with clinical applications: A programmed approach (7th ed.). Clifton Park, NY: Delmar Learning.
2. Smeltzer, S. C., & Bare, B. G. (2004). Brunner and Suddarth's textbook of medical-surgical nursing (10th ed.). Philadelphia: Lippincott, Williams and Wilkins.
3. Chiasson, J. L., Aris-Jilwan, N., et al. (2003). Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ, 168(7), 159.
4. Luckey, A. E., & Parsa, C. J. (2003). Fluid and electrolytes in the aged. Arch Surg, 138(10), 1055.
5. Metheny, N. M. (2000). Fluid and electrolyte balance nursing considerations (4th ed.). Philadelphia: Lippincott.
6. Johnson, A. L., & Criddle, L. M. (2004). Pass the salt. Crit Care Nurse, 24(5), 36.
7. Dacey, M. J. (2001). Hypomagnesemic disorders. Crit Care Clin, 17(1), 155.
Wednesday, January 19, 2011
IV fluids: Do you know what's hanging and why?Publish date: Oct 1, 2007
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Originally Posted October 2007
By KIM DAVID, RN, MSN
KIM DAVID is the education coordinator at Rockdale Medical Center, Conyers, GA. The author has no financial relationships to disclose. STAFF EDITOR: TERRI J. METULES, RN, BSN
New evidence calls for a review of fluid therapy.
Why is water so important? It comprises 55% – 65% of an average adult's body weight.1 A newborn is about 95% water; an elderly or obese person, around 40%.1 A loss of body water, whether acute or chronic, can cause a range of problems from mild lightheadedness to convulsions, coma, and in some cases, death.2
That's why many hospitalized patients have some type of intravenous fluid therapy as part of their care. Some need fluid to maintain water balance; others require it as replacement or restorative therapy.
Though fluid therapy can be a lifesaver, it's not innocuous. Giving the wrong fluid can be deadly. Since there are more than a hundred different types of IV fluids that vary in effect, you need a simple way to keep them straight. Here, we'll review the principles that govern fluid therapy and give you an update on the latest evidence regarding its use.
How the body's water is distributed
Water is found in two major body compartments: inside (intracellular) and outside (extracellular) the cells. While cells hold two-thirds of the body's water, the remaining one-third is divided between the vascular and interstitial spaces; one-quarter of it is found in the vessels, and the remainder is in the interstitium.1,2
Because the walls that separate these compartments are porous, water moves freely between them.2 The tiny pores that line the walls of the cells and capillaries also let small particles like sodium and chloride pass through easily.
Large molecules like proteins and starches usually stay put. But a "two-pore theory" suggests that there are some larger pores along the venous capillaries that let big particles pass into the interstitial space.3 This theory is used to explain why some of our efforts to expand blood volume following trauma tend to fail.
Forces that move water
Hydrostatic and osmotic pressures, along with hormones, tightly regulate the body's water. Intravenous fluid therapy primarily manipulates these two types of pressure. Hydrostatic pressure simply reflects the weight and volume of water: The more volume, the higher the blood pressure. That's why fluids are given to patients in shock;4 increasing the intravascular volume raises blood pressure, which helps keep vital organs perfused.
But this strategy has a downside: Think of a balloon partly filled with water. Make it semipermeable with tiny pinpricks and watch it drip. Then add more water to the balloon and watch the rise in hydrostatic pressure cause the drip to become a spray.
Giving a large volume of IV fluid has the same effect on circulation. The weight stretches the vascular pores, allowing fluid and all sizes of particles to quickly escape from the vessels.3 In fact, about 75% of a normal saline (NS) bolus leaves the vascular bed instantly.5 The edema that results from aggressive saline administration is linked to poor outcomes in trauma patients.4
Fluid therapy also affects osmotic pressure. Osmosis is often defined as "the diffusion of water across a semipermeable membrane from an area of high concentration to an area of low concentration."6 But it may be easier to understand when put this way: Water moves into the compartment with the higher concentration of particles, or solute. Water is actually pulled into the compartment in the same way that a sponge soaks up a spill. This pull is called osmotic pressure.
While the size of particles distinguishes the two major types of fluid—crystalloid (small) or colloid (large)—it's the number of particles in each compartment that keeps water where it's supposed to be.6 Nurses give fluids with more (or fewer) particles than blood plasma to pull fluid into the compartment that needs it most.
So how do you know where the water is needed? To assess water balance, you'll measure the osmolality of blood plasma. Osmolality is the number of particles (osmoles) in a kilogram of fluid; osmolarity is the number of particles in a liter of fluid. These terms are often used interchangeably because the density of water is 1 kg/L. Normal serum osmolality is around 300 mOsm/L.1,4
Crystalloids come in three tonicities
Crystalloids are so named because they are made of substances that form crystals. Salt is a perfect example. Its crystals readily form out of particles of sodium and chloride, and then dissociate in water. Because the particles are small, weighing around 30 kilodaltons (kDa),3 they can easily pass in and out of the pores between compartments.
Crystalloids are categorized by their tonicity, a synonym for osmolality. A fluid that's isotonic has the same number of particles—the same osmolality—as plasma. Therefore, an isotonic solution won't promote the shift of fluids into or out of the cells, causing them to swell or shrink. Isotonic crystalloids shouldn't cause edema, either, and usually don't when given in moderation.
Normal saline (0.9%) and lactated Ringer's (LR) solution are two of the most commonly used isotonic fluids. They're currently the mainstay of resuscitation therapy,4,7 and are often used for electrolyte replacement and for perioperative fluid administration.8,9
New evidence suggests that these fluids may do more harm than originally thought.9,10 (For a summary of fluid research, see "The fluid controversy heats up" at the end of this article.) While fluid overload has always been a concern when giving IV fluids, research now shows that isotonic crystalloids are proinflammatory.10 Lactated Ringer's, in particular, activates neutrophils, which destroy surrounding tissue by way of oxidative burst—the process whereby a neutrophil undergoes apoptosis, or programmed cell death, and spews its contents, including hydrogen peroxide, into surrounding tissue.10,11 This process may be the trigger for acute respiratory distress syndrome (ARDS).11,12
Dextrose 5% in water (D5W) is another isotonic crystalloid. However, it's not used for resuscitation because, as its glucose is metabolized, this fluid quickly becomes hypotonic. In fact, D5W is a good source of free water.1 As with other hypotonic fluids, such as 0.45% NS, the water quickly shifts out of the vascular bed and into the cells, by way of osmosis.
Nurses frequently give hypotonic fluids to correct cellular dehydration and hypernatremia.1 Give them with caution, however, because as they shift water out of the vascular bed, hypotonic fluids can worsen hypotension in a patient with low blood pressure.1
Hypertonic fluids, on the other hand, have more particles than the body's water. They pull water back into circulation from the cells and interstitial spaces, which can shrink the cells.12,13 These fluids are also used to correct electrolyte imbalances. Hypertonic saline has an additional benefit: It suppresses inflammation. That's one reason it's gaining respect as a resuscitation fluid of first choice.10,12
Colloids 101: The other fluids
Unlike in crystalloids, the particles suspended in colloids don't break down into smaller pieces in water. Most of them are larger than 30 kDa, so they won't fit through most capillary pores. Therefore, colloids tend to stay in the vascular bed,3 which is why they are used for volume expansion.
The advantage of administering colloids is that you can give smaller amounts of fluid (about 250 ml) and achieve the same effect you would with four liters of crystalloids.10 However, the downside is that, as hydrostatic pressure rises in the capillaries, the pores stretch and let colloids pass through.3 The edema that results takes longer to resolve than that produced by crystalloids.
Commonly used colloids include human albumin, a natural protein that's separated from plasma; hetastarch (HES), a synthetic starch derived from hydroxyethyl glucose; mannitol, an alcohol sugar; and dextran, a polysaccharide. These and other frequently used IV solutions are listed in the table at the bottom of this article, along with their actions, uses, and nursing considerations.
Like crystalloids, colloids are linked to a number of complications. Fluid overload is common to both types of fluid. Specifically, albumin is linked to anaphylaxis and pulmonary edema; HES and dextran are associated with a range of hypersensitivity reactions and bleeding. What's more, mannitol, traditionally used to treat increased intracranial pressure (ICP), can actually raise ICP and increase cerebral edema.
Monitoring therapy: What to watch for
Before you hang any IV fluid, know what you're hanging, why it's been ordered, and what complications may occur. Since fluid overload is common to all IV solutions, be alert for its signs: neck vein distention, increased blood pressure, adventitious lung sounds, and respiratory distress.
Monitor fluid balance by checking intake and output at least every shift to make sure the kidneys are functioning properly. Weigh your patient daily and assess vital signs regularly, watching for trends such as weight gain, increasing blood pressure, or a rise in heart or respiratory rate.
If you suspect volume overload, discontinue the fluid immediately, and give supplemental oxygen and diuretics as ordered. If the patient is having trouble breathing, elevating the head of the bed may help.
When infusing LR, be sure to monitor the patient's electrolyte levels. Watch especially for a rise in potassium, which can lead to cardiac dysrhythmias. If the potassium is seriously high, you may need to give calcium chloride. Another antidote is insulin, given with 50% dextrose. As insulin drives glucose into the cells, it activates the sodium-potassium pump, which moves potassium back into the cells as well.
Likewise, you should monitor serum sodium levels in patients receiving NS or hypertonic saline solutions.1,2 Because an excess of serum sodium causes brain cells to shrink, most of the early signs of hypernatremia are neurological: muscle weakness, twitching, personality changes, agitation, and hallucinations. Hypotonic or isotonic fluids are the treatment of choice.
On the flip side, hyponatremia can result from disease or hypotonic saline or dextrose solutions. Here, brain cells swell. Signs include headache, weakness, nervousness, vomiting, tremor, convulsions, and coma. The patient's pupils may be dilated, and you may also note Babinski's sign. Most cases of hyponatremia occur in postop women and small children.2 The condition is usually treated with hypertonic saline.
Other complications of fluid therapy include phlebitis, infiltration, and extravasation. Many IV fluids are irritating to the veins, so if you note redness and swelling at or along the IV site, discontinue the fluid and remove the IV immediately. Then apply warm compresses, and restart the infusion at another site.
Infiltration occurs when IV fluid leaks into the tissue surrounding the IV site. It's caused by improper catheter placement, or by dislodgement of the catheter—typically, from patient movement. Most of the time, infiltration of a nonirritating fluid won't cause any harm, though a large amount of any fluid can cause tissue damage.
Extravasation is a more serious type of infiltration. It's caused by a vesicant—an IV fluid (or drug) that can irritate the vein walls, trigger vasoconstriction, or cause the vein to rupture. Examples include IV potassium, calcium, magnesium, or 20% – 50% dextrose. Pain, infection, and severe tissue necrosis may result. If you suspect extravasation, stop the infusion and call the physician immediately to determine the next step.
Most of the time, IV therapy does more good than harm. Knowing the different types of solutions, as well as their uses and adverse effects, will help ensure that you administer these fluids safely and appropriately.
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REFERENCES
1. Subramanian, S., & Ziedalski, T. M. (2005). Oliguria, volume overload, Na+ balance, and diuretics. Crit Care Clin, 21(2), 291.
2. Lin, M., Liu, S. J., & Lim, I. T. (2005). Disorders of water imbalance. Emerg Med Clin North Am, 23(3), 749.
3. Persson, J., & Grände, P. O. (2006). Plasma volume expansion and transcapillary fluid exchange in skeletal muscle of albumin, dextran, gelatin, hydroxyethyl starch, and saline after trauma in the cat. Crit Care Med, 34(9), 2456.
4. Mizushima, Y., Tohira, H., et al. (2005). Fluid resuscitation of trauma patients: How fast is the optimal rate? Am J Emerg Med, 23(7), 833.
5. Hirshberg, A., Hoyt, D. B., & Mattox, K. L. (2007). From leaky buckets to vascular injuries: Understanding models of uncontrolled hemorrhage. J Am Coll Surg, 204(4), 665.
6. Sterns, R. H. "Disorders of water and sodium balance: Introduction." 2002. www.medscape.com/viewarticle/535477 (3 Aug. 2007).
7. Bulger, E. M., & Maier, R. V. (2007). Prehospital care of the injured: What's new. Surg Clin North Am, 87(1), 37.
8. Deitch, E. A., Dayal, S. D., & Delinger, R. P. (2006). Intensive care unit management of the trauma patient. Crit Care Med, 34(9), 2294.
9. Holte, K., & Kehlet, H. (2006). Fluid therapy and surgical outcome in elective surgery: A need for reassessment in fast-track surgery. Am Coll Surgeons, 202(6), 971.
10. Alam, H. B., & Rhee, P. (2007). New developments in fluid resuscitation. Surg Clin North Am, 87(1), 55.
11. Macintyre, N. "Fluid management in patients with ALI from the NIH ARDS Network fluid management trial." 2006. www.medscape.com/viewarticle/543504 (3 Aug. 2007).
12. Beekley, A. C., Starnes, B. W., & Sebesta, J. A. (2007). Lessons learned from modern military surgery. Surg Clin North Am, 87(1), 157.
13. Toung, T. J. K., Chen, C. H., et al. (2007). Osmotherapy with hypertonic saline attenuates water content in the brain and extracerebral organs. Crit Care Med, 35(2), 526.
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The fluid controversy heats up
There are tons of studies on fluids, none of them conclusive. We need to standardize our research efforts or the fluid controversy will never come to a close. Here's a brief look at the evidence we've got to date:
Fluids for resuscitation
The standard amount of crystalloids recommended for trauma victims—three to eight times the estimated blood loss—came under scrutiny once researchers found a higher mortality rate among patients who received fluids than those who did not. Limiting fluids, called permissive hypotension, is now the trend.
"Less is more" works except in cases of traumatic brain injury, where hypotension can cause brain damage.
Nevertheless, studies show that aggressive and excessive fluid resuscitation with isotonic crystalloids reduces oxygenation by diluting hemoglobin and stimulating rebleeding. It also promotes coagulopathy, abdominal compartment syndrome, and hypochloremic acidosis.
Crystalloids, particularly lactated Ringer's solution, can accelerate systemic inflammation in trauma patients by activating neutrophils. Research shows that it's the body's neutrophils that spark the diffuse cellular injury that leads to acute respiratory distress syndrome and multiple organ failure (MOF).
Because of these dangers, there's a renewed interest in hypertonic saline (HS) with or without dextran as a resuscitation fluid of first choice. The major advantage of HS is that it can expand volume using as little as 250 ml of fluid. But the best part is the finding that HS decreases neutrophil activation, blunts inflammation, and helps prevent lung and bowel injury.
The future may bring gene therapy to stop inflammation, improved blood substitutes to support oxygenation, and designer fluids with antioxidants to decrease reperfusion injury. You may also see splanchnic-directed therapy to prevent MOF.
Perioperative fluid therapy
The current recommendations for administering perioperative fluid therapy are based on studies of critically ill patients. New evidence suggests that this practice may be detrimental, and that both the type and amount of fluid affect surgical outcomes.
Because stress causes the body to hang onto water and increases capillary permeability, surgical patients are prone to weight gain. Those undergoing major surgery have a marked stress response. Giving these patients lots of fluid (>5 L) promotes significant third-spacing. Those who received a large volume of fluid had more cardiac and pulmonary complications from fluid overload. The most common were pulmonary edema, atelectasis, and pneumonia. They also experienced decreased gastric motility and prolonged ileus.
While the amount of fluid had no effect on wound healing in these patients, limiting fluids proved to significantly shorten postop ileus and improve tissue oxygenation. The goal for fluid therapy in major surgery should be to optimize cardiac and pulmonary function, shorten postop ileus, and avoid renal problems.
Patients undergoing minor and moderate procedures benefited from receiving one to three liters of fluid. Those who were restricted to one liter or less had more nausea and vomiting and dizziness. Bottom line: less is more, some is better than none.
Sources: 1. Alam, H. B., & Rhee, P. (2007). New developments in fluid resuscitation. Surg Clin North Am, 87(1), 55. 2. Beekley, A. C., Starnes, B. W., & Sebesta, J. A. (2007). Lessons learned from modern military surgery. Surg Clin North Am, 87(1), 157. 3. Bulger, E. M., & Maier, R. V. (2007). Prehospital care of the injured: What's new. Surg Clin North Am, 87(1), 37. 4. Deitch, E. A., Dayal, S. D., & Delinger, R. P. (2006). Intensive care unit management of the trauma patient. Crit Care Med, 34(9), 2294. 5. Holte, K., & Kehlet, H. (2006). Fluid therapy and surgical outcome in elective surgery: A need for reassessment in fast-track surgery. Am Coll Surgeons, 202(6), 971. 6. Macintyre, N. "Fluid management in patients with ALI from the NIH ARDS Network fluid management trial." 2006. www.medscape.com/viewarticle/543504. (3 Aug 2007).
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Originally Posted October 2007
By KIM DAVID, RN, MSN
KIM DAVID is the education coordinator at Rockdale Medical Center, Conyers, GA. The author has no financial relationships to disclose. STAFF EDITOR: TERRI J. METULES, RN, BSN
New evidence calls for a review of fluid therapy.
Why is water so important? It comprises 55% – 65% of an average adult's body weight.1 A newborn is about 95% water; an elderly or obese person, around 40%.1 A loss of body water, whether acute or chronic, can cause a range of problems from mild lightheadedness to convulsions, coma, and in some cases, death.2
That's why many hospitalized patients have some type of intravenous fluid therapy as part of their care. Some need fluid to maintain water balance; others require it as replacement or restorative therapy.
Though fluid therapy can be a lifesaver, it's not innocuous. Giving the wrong fluid can be deadly. Since there are more than a hundred different types of IV fluids that vary in effect, you need a simple way to keep them straight. Here, we'll review the principles that govern fluid therapy and give you an update on the latest evidence regarding its use.
How the body's water is distributed
Water is found in two major body compartments: inside (intracellular) and outside (extracellular) the cells. While cells hold two-thirds of the body's water, the remaining one-third is divided between the vascular and interstitial spaces; one-quarter of it is found in the vessels, and the remainder is in the interstitium.1,2
Because the walls that separate these compartments are porous, water moves freely between them.2 The tiny pores that line the walls of the cells and capillaries also let small particles like sodium and chloride pass through easily.
Large molecules like proteins and starches usually stay put. But a "two-pore theory" suggests that there are some larger pores along the venous capillaries that let big particles pass into the interstitial space.3 This theory is used to explain why some of our efforts to expand blood volume following trauma tend to fail.
Forces that move water
Hydrostatic and osmotic pressures, along with hormones, tightly regulate the body's water. Intravenous fluid therapy primarily manipulates these two types of pressure. Hydrostatic pressure simply reflects the weight and volume of water: The more volume, the higher the blood pressure. That's why fluids are given to patients in shock;4 increasing the intravascular volume raises blood pressure, which helps keep vital organs perfused.
But this strategy has a downside: Think of a balloon partly filled with water. Make it semipermeable with tiny pinpricks and watch it drip. Then add more water to the balloon and watch the rise in hydrostatic pressure cause the drip to become a spray.
Giving a large volume of IV fluid has the same effect on circulation. The weight stretches the vascular pores, allowing fluid and all sizes of particles to quickly escape from the vessels.3 In fact, about 75% of a normal saline (NS) bolus leaves the vascular bed instantly.5 The edema that results from aggressive saline administration is linked to poor outcomes in trauma patients.4
Fluid therapy also affects osmotic pressure. Osmosis is often defined as "the diffusion of water across a semipermeable membrane from an area of high concentration to an area of low concentration."6 But it may be easier to understand when put this way: Water moves into the compartment with the higher concentration of particles, or solute. Water is actually pulled into the compartment in the same way that a sponge soaks up a spill. This pull is called osmotic pressure.
While the size of particles distinguishes the two major types of fluid—crystalloid (small) or colloid (large)—it's the number of particles in each compartment that keeps water where it's supposed to be.6 Nurses give fluids with more (or fewer) particles than blood plasma to pull fluid into the compartment that needs it most.
So how do you know where the water is needed? To assess water balance, you'll measure the osmolality of blood plasma. Osmolality is the number of particles (osmoles) in a kilogram of fluid; osmolarity is the number of particles in a liter of fluid. These terms are often used interchangeably because the density of water is 1 kg/L. Normal serum osmolality is around 300 mOsm/L.1,4
Crystalloids come in three tonicities
Crystalloids are so named because they are made of substances that form crystals. Salt is a perfect example. Its crystals readily form out of particles of sodium and chloride, and then dissociate in water. Because the particles are small, weighing around 30 kilodaltons (kDa),3 they can easily pass in and out of the pores between compartments.
Crystalloids are categorized by their tonicity, a synonym for osmolality. A fluid that's isotonic has the same number of particles—the same osmolality—as plasma. Therefore, an isotonic solution won't promote the shift of fluids into or out of the cells, causing them to swell or shrink. Isotonic crystalloids shouldn't cause edema, either, and usually don't when given in moderation.
Normal saline (0.9%) and lactated Ringer's (LR) solution are two of the most commonly used isotonic fluids. They're currently the mainstay of resuscitation therapy,4,7 and are often used for electrolyte replacement and for perioperative fluid administration.8,9
New evidence suggests that these fluids may do more harm than originally thought.9,10 (For a summary of fluid research, see "The fluid controversy heats up" at the end of this article.) While fluid overload has always been a concern when giving IV fluids, research now shows that isotonic crystalloids are proinflammatory.10 Lactated Ringer's, in particular, activates neutrophils, which destroy surrounding tissue by way of oxidative burst—the process whereby a neutrophil undergoes apoptosis, or programmed cell death, and spews its contents, including hydrogen peroxide, into surrounding tissue.10,11 This process may be the trigger for acute respiratory distress syndrome (ARDS).11,12
Dextrose 5% in water (D5W) is another isotonic crystalloid. However, it's not used for resuscitation because, as its glucose is metabolized, this fluid quickly becomes hypotonic. In fact, D5W is a good source of free water.1 As with other hypotonic fluids, such as 0.45% NS, the water quickly shifts out of the vascular bed and into the cells, by way of osmosis.
Nurses frequently give hypotonic fluids to correct cellular dehydration and hypernatremia.1 Give them with caution, however, because as they shift water out of the vascular bed, hypotonic fluids can worsen hypotension in a patient with low blood pressure.1
Hypertonic fluids, on the other hand, have more particles than the body's water. They pull water back into circulation from the cells and interstitial spaces, which can shrink the cells.12,13 These fluids are also used to correct electrolyte imbalances. Hypertonic saline has an additional benefit: It suppresses inflammation. That's one reason it's gaining respect as a resuscitation fluid of first choice.10,12
Colloids 101: The other fluids
Unlike in crystalloids, the particles suspended in colloids don't break down into smaller pieces in water. Most of them are larger than 30 kDa, so they won't fit through most capillary pores. Therefore, colloids tend to stay in the vascular bed,3 which is why they are used for volume expansion.
The advantage of administering colloids is that you can give smaller amounts of fluid (about 250 ml) and achieve the same effect you would with four liters of crystalloids.10 However, the downside is that, as hydrostatic pressure rises in the capillaries, the pores stretch and let colloids pass through.3 The edema that results takes longer to resolve than that produced by crystalloids.
Commonly used colloids include human albumin, a natural protein that's separated from plasma; hetastarch (HES), a synthetic starch derived from hydroxyethyl glucose; mannitol, an alcohol sugar; and dextran, a polysaccharide. These and other frequently used IV solutions are listed in the table at the bottom of this article, along with their actions, uses, and nursing considerations.
Like crystalloids, colloids are linked to a number of complications. Fluid overload is common to both types of fluid. Specifically, albumin is linked to anaphylaxis and pulmonary edema; HES and dextran are associated with a range of hypersensitivity reactions and bleeding. What's more, mannitol, traditionally used to treat increased intracranial pressure (ICP), can actually raise ICP and increase cerebral edema.
Monitoring therapy: What to watch for
Before you hang any IV fluid, know what you're hanging, why it's been ordered, and what complications may occur. Since fluid overload is common to all IV solutions, be alert for its signs: neck vein distention, increased blood pressure, adventitious lung sounds, and respiratory distress.
Monitor fluid balance by checking intake and output at least every shift to make sure the kidneys are functioning properly. Weigh your patient daily and assess vital signs regularly, watching for trends such as weight gain, increasing blood pressure, or a rise in heart or respiratory rate.
If you suspect volume overload, discontinue the fluid immediately, and give supplemental oxygen and diuretics as ordered. If the patient is having trouble breathing, elevating the head of the bed may help.
When infusing LR, be sure to monitor the patient's electrolyte levels. Watch especially for a rise in potassium, which can lead to cardiac dysrhythmias. If the potassium is seriously high, you may need to give calcium chloride. Another antidote is insulin, given with 50% dextrose. As insulin drives glucose into the cells, it activates the sodium-potassium pump, which moves potassium back into the cells as well.
Likewise, you should monitor serum sodium levels in patients receiving NS or hypertonic saline solutions.1,2 Because an excess of serum sodium causes brain cells to shrink, most of the early signs of hypernatremia are neurological: muscle weakness, twitching, personality changes, agitation, and hallucinations. Hypotonic or isotonic fluids are the treatment of choice.
On the flip side, hyponatremia can result from disease or hypotonic saline or dextrose solutions. Here, brain cells swell. Signs include headache, weakness, nervousness, vomiting, tremor, convulsions, and coma. The patient's pupils may be dilated, and you may also note Babinski's sign. Most cases of hyponatremia occur in postop women and small children.2 The condition is usually treated with hypertonic saline.
Other complications of fluid therapy include phlebitis, infiltration, and extravasation. Many IV fluids are irritating to the veins, so if you note redness and swelling at or along the IV site, discontinue the fluid and remove the IV immediately. Then apply warm compresses, and restart the infusion at another site.
Infiltration occurs when IV fluid leaks into the tissue surrounding the IV site. It's caused by improper catheter placement, or by dislodgement of the catheter—typically, from patient movement. Most of the time, infiltration of a nonirritating fluid won't cause any harm, though a large amount of any fluid can cause tissue damage.
Extravasation is a more serious type of infiltration. It's caused by a vesicant—an IV fluid (or drug) that can irritate the vein walls, trigger vasoconstriction, or cause the vein to rupture. Examples include IV potassium, calcium, magnesium, or 20% – 50% dextrose. Pain, infection, and severe tissue necrosis may result. If you suspect extravasation, stop the infusion and call the physician immediately to determine the next step.
Most of the time, IV therapy does more good than harm. Knowing the different types of solutions, as well as their uses and adverse effects, will help ensure that you administer these fluids safely and appropriately.
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REFERENCES
1. Subramanian, S., & Ziedalski, T. M. (2005). Oliguria, volume overload, Na+ balance, and diuretics. Crit Care Clin, 21(2), 291.
2. Lin, M., Liu, S. J., & Lim, I. T. (2005). Disorders of water imbalance. Emerg Med Clin North Am, 23(3), 749.
3. Persson, J., & Grände, P. O. (2006). Plasma volume expansion and transcapillary fluid exchange in skeletal muscle of albumin, dextran, gelatin, hydroxyethyl starch, and saline after trauma in the cat. Crit Care Med, 34(9), 2456.
4. Mizushima, Y., Tohira, H., et al. (2005). Fluid resuscitation of trauma patients: How fast is the optimal rate? Am J Emerg Med, 23(7), 833.
5. Hirshberg, A., Hoyt, D. B., & Mattox, K. L. (2007). From leaky buckets to vascular injuries: Understanding models of uncontrolled hemorrhage. J Am Coll Surg, 204(4), 665.
6. Sterns, R. H. "Disorders of water and sodium balance: Introduction." 2002. www.medscape.com/viewarticle/535477 (3 Aug. 2007).
7. Bulger, E. M., & Maier, R. V. (2007). Prehospital care of the injured: What's new. Surg Clin North Am, 87(1), 37.
8. Deitch, E. A., Dayal, S. D., & Delinger, R. P. (2006). Intensive care unit management of the trauma patient. Crit Care Med, 34(9), 2294.
9. Holte, K., & Kehlet, H. (2006). Fluid therapy and surgical outcome in elective surgery: A need for reassessment in fast-track surgery. Am Coll Surgeons, 202(6), 971.
10. Alam, H. B., & Rhee, P. (2007). New developments in fluid resuscitation. Surg Clin North Am, 87(1), 55.
11. Macintyre, N. "Fluid management in patients with ALI from the NIH ARDS Network fluid management trial." 2006. www.medscape.com/viewarticle/543504 (3 Aug. 2007).
12. Beekley, A. C., Starnes, B. W., & Sebesta, J. A. (2007). Lessons learned from modern military surgery. Surg Clin North Am, 87(1), 157.
13. Toung, T. J. K., Chen, C. H., et al. (2007). Osmotherapy with hypertonic saline attenuates water content in the brain and extracerebral organs. Crit Care Med, 35(2), 526.
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The fluid controversy heats up
There are tons of studies on fluids, none of them conclusive. We need to standardize our research efforts or the fluid controversy will never come to a close. Here's a brief look at the evidence we've got to date:
Fluids for resuscitation
The standard amount of crystalloids recommended for trauma victims—three to eight times the estimated blood loss—came under scrutiny once researchers found a higher mortality rate among patients who received fluids than those who did not. Limiting fluids, called permissive hypotension, is now the trend.
"Less is more" works except in cases of traumatic brain injury, where hypotension can cause brain damage.
Nevertheless, studies show that aggressive and excessive fluid resuscitation with isotonic crystalloids reduces oxygenation by diluting hemoglobin and stimulating rebleeding. It also promotes coagulopathy, abdominal compartment syndrome, and hypochloremic acidosis.
Crystalloids, particularly lactated Ringer's solution, can accelerate systemic inflammation in trauma patients by activating neutrophils. Research shows that it's the body's neutrophils that spark the diffuse cellular injury that leads to acute respiratory distress syndrome and multiple organ failure (MOF).
Because of these dangers, there's a renewed interest in hypertonic saline (HS) with or without dextran as a resuscitation fluid of first choice. The major advantage of HS is that it can expand volume using as little as 250 ml of fluid. But the best part is the finding that HS decreases neutrophil activation, blunts inflammation, and helps prevent lung and bowel injury.
The future may bring gene therapy to stop inflammation, improved blood substitutes to support oxygenation, and designer fluids with antioxidants to decrease reperfusion injury. You may also see splanchnic-directed therapy to prevent MOF.
Perioperative fluid therapy
The current recommendations for administering perioperative fluid therapy are based on studies of critically ill patients. New evidence suggests that this practice may be detrimental, and that both the type and amount of fluid affect surgical outcomes.
Because stress causes the body to hang onto water and increases capillary permeability, surgical patients are prone to weight gain. Those undergoing major surgery have a marked stress response. Giving these patients lots of fluid (>5 L) promotes significant third-spacing. Those who received a large volume of fluid had more cardiac and pulmonary complications from fluid overload. The most common were pulmonary edema, atelectasis, and pneumonia. They also experienced decreased gastric motility and prolonged ileus.
While the amount of fluid had no effect on wound healing in these patients, limiting fluids proved to significantly shorten postop ileus and improve tissue oxygenation. The goal for fluid therapy in major surgery should be to optimize cardiac and pulmonary function, shorten postop ileus, and avoid renal problems.
Patients undergoing minor and moderate procedures benefited from receiving one to three liters of fluid. Those who were restricted to one liter or less had more nausea and vomiting and dizziness. Bottom line: less is more, some is better than none.
Sources: 1. Alam, H. B., & Rhee, P. (2007). New developments in fluid resuscitation. Surg Clin North Am, 87(1), 55. 2. Beekley, A. C., Starnes, B. W., & Sebesta, J. A. (2007). Lessons learned from modern military surgery. Surg Clin North Am, 87(1), 157. 3. Bulger, E. M., & Maier, R. V. (2007). Prehospital care of the injured: What's new. Surg Clin North Am, 87(1), 37. 4. Deitch, E. A., Dayal, S. D., & Delinger, R. P. (2006). Intensive care unit management of the trauma patient. Crit Care Med, 34(9), 2294. 5. Holte, K., & Kehlet, H. (2006). Fluid therapy and surgical outcome in elective surgery: A need for reassessment in fast-track surgery. Am Coll Surgeons, 202(6), 971. 6. Macintyre, N. "Fluid management in patients with ALI from the NIH ARDS Network fluid management trial." 2006. www.medscape.com/viewarticle/543504. (3 Aug 2007).
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