Fluid Replacement - Pharmacology

The amount of water a patient requires each day depends on the patient’s age and the nature of the patient’s medical condition. Water is 30 mL/kg of body weight.

A patient who weighs 70 kg has 2100 mL of water (70 kg x 30 mL/kg). In other words, a patient who weighs 150 lbs weighs 68 kg (150 lbs/2.2 lbs/kg) and has 2240 mL of water.

Each day the patient losses:

  • 400 mL to 500 mL of water through evaporation from the skin.
  • 400 mL to 500 mL of water through breathing.
  • 100 mL to 200 mL of water in feces.
  • 1000 mL to 1200 mL of water in urine.

This means that each day the patient must take in between 1900 mL and 2400 mL of fluid in order to maintain fluid-electrolyte balance. However, disease and the treatment of disease can increase the patient’s output of water requiring that the patient increase the intake of water.

For example, a patient who has a fever loses as much as 15% more water than the normal daily water loss. That is, the patient loses between 2185 mL and 2760 mL of water each day when he or she has a fever.


When a patient is experiencing the loss of fluid, the nurse should:

  • Establish baseline vital signs and weight.
  • Review lab results and report elevations in the hematocrit and BUN. If both values are elevated this could indicate the patient is dehydrated. If the BUN is >60 mg/dL, renal impairment may be the cause.
  • Measure urine output. Report if output is (30 mL/h or 600 mL/day. Normal urine output should be)35 mL/h or 1000 to 1200 mL/day.
  • Review the lab results for urine specific gravity (SG). Normal range is 1.005 to 1.030. If the SG is greater than 1.030, dehydration may be the cause.
  • Verify that the proper osmolality of the IV fluids are ordered. If there is continuous use of one type of IV fluid such as 5% dextrose in water (D5W), hypo-osmolality of body fluid could occur.

Potential nursing diagnoses for a patient that is receiving fluid volume replacement therapy are:

  • Risk for fluid volume excess. This can occur when the patient is given too much replacement fluid, fluid is infused too rapidly, or the volume is too much for the patient’s physical size or condition.
  • Risk for fluid volume deficit related to inadequate fluid intake.
  • Altered tissue perfusion, related to decreased blood circulation or inade-quate fluid replacement.

Before beginning fluid replacement therapy, goals should include:

  • Patient will not develop fluid volume deficit or excess as a result of IV fluid replacement.
  • Patient will remain hydrated.
  • Vital signs and urine output will remain in normal ranges.

When fluid replacement therapy is underway, make sure to monitor:

  • Vital signs.
  • Fluid intake and output.
  • Daily weight.
  • Signs and symptoms of fluid volume excess (overload) which include cough, dyspnea (difficulty breathing), jugular vein distention (JVD) (neck vein engorgement), moistrales (abnormal breath sounds).
  • Signs and symptoms of fluid volume deficit (dehydration) which include thirst, dry mucous membranes, poor skin turgor, decreased urine output, tachycardia, slight decrease in systolic blood pressure.
  • Lab results especially BUN, hemoglobin and hematocrit.
  • Types of IV fluids being infused.
  • IV site for infiltration or phlebitis.

The patient should be taught:

  • To recognize signs and symptoms of fluid volume excess and fluid volume deficit.
  • How to measure fluid intake and output.
  • How to weigh himself or herself.

The nurse must frequently evaluate the patient’s

  • Urine output (normal limits).
  • Breath sounds (normal limits).
  • Lab results (normal limits).
  • Vital signs (normal limits).
  • Weight (not increased).
  • Skin turgor (normal).
  • IV site (should not be red, swollen, hot or hard).
  • IV patency (should be flowing as per the set drip rate).


Potassium is an electrolyte cation that is more prevalent inside cells than it is in extra cellular fluid. It is used to transmit and conduct neurological impulses and to maintain cardiac rhythms. Potassium is also used to contract skeletal and smooth muscles.

In order for a muscle to contract, the concentration of potassium inside the cell moves out and is replaced by sodium, which is the prevalent electrolyte outside the cell (see Sodium). These electrolytes reverse position when the muscle re polarizes. The concentration of potassium and sodium is maintained by the sodium-potassium pump found in cell membranes. The sodium-potassium pump uses adenosine triphosphate (ATP) to pump potassium back into the cell and sodium out of the cell.

Potassium regulates intracellular osmolality and promotes cell growth. It moves into cells as new tissues form and leaves cells when tissues break down. Patients receive potassium from their diet and excrete potassium in urine (90%) and feces (8%).

Serum potassium is measured to determine if the patient has a normal range of potassium. The normal serum potassium is between 3.5 to 5.3 milliequiva-lents per liter (mEq/L). Caution: Serum potassium less than 2.5 mEq/L or greater than 7.0 mEq/L can cause the patient to have a cardiac arrest. Diseases such as kidney disease can cause potassium to become imbalanced. When this happens, the patient will exhibit specific signs and symptoms and the serum potassium will be outside the normal range.


Hyperkalemia occurs when a patient has a serum potassium level greater than 5.3 mEq/L. A number of factors can cause this condition including:

  • Impaired renal excretion (most common).
  • Massive intake of potassium.
  • Medications such as potassium-sparing diuretics Aldactone and Dyrenium, angiotensin-converting enzyme (ACE) inhibitors Vasotec and Prinivil, which reduce the kidney’s ability to secrete potassium.

The nurse should monitor a patient for the signs and symptoms of hyperkalemia. The more common of these are:

  • Nausea.
  • Cold skin; grayish pallor.
  • Hypotension.
  • Mental confusion and irritability.
  • Abdominal cramps.
  • Oliguria (decreased urine output).
  • Tachycardia (fast pulse) and later bradycardia (slow pulse).
  • Muscle weakness to flaccid paralysis.
  • Numbness or tingling in the extremities.
  • Peaked T waves on the EKG.

The nurse must respond quickly once signs and symptoms of hyperkalemia develop as the patient is at risk for seizures, injury related to muscle weakness, and cardiac arrhythmias. Here is what needs to be done.

  • Restrict intake of potassium rich foods.
  • Administer diuretics and ion-exchange resins such as Kayexalate (reten-tion enema) as directed to increase the elimination of potassium.
  • Dialysis therapy may be ordered in critical cases to remove potassium.
  • Administer insulin and glucose parenterally to force potassium back inside cells.
  • Administer sodium bicarbonate intravenously to correct the acidosis (ele-vate pH).
  • Administer calcium gluconate intravenously to decrease the irritability of the heart; it does not promote potassium loss.


Hypokalemia occurs when a patient has a serum potassium level of less than 3.5 mEq/L. A number of factors can cause this condition. These include:

  • Diarrhea.
  • Vomiting.
  • Fistulas.
  • Nasogastric suctionings.
  • Diuretics.
  • Hyperaldosteronism.
  • Magnesium depletion.
  • Diaphoresis.
  • Dialysis.
  • Increased insulin.
  • Alkalosis.
  • Stress (increases epinephrine).
  • Starvation.
  • Low potassium in diet.

The patient may have the following signs and symptoms when experiencing hypokalemia:

  • Leg cramps.
  • Muscle weakness.
  • Vomiting.
  • Fatigue.
  • Decreased reflexes.
  • Polyuria.
  • Irregular pulse.
  • Bradycardia.

The patient may also exhibit an abnormal EKG that shows:

  • Depressed ST segment.
  • Flattened T wave.
  • Presence of U wave.
  • Premature ventricular contractions.

The nurse must respond with the following interventions as the patient is a risk for injury related to muscle weakness and cardiac arrhythmias.

  • Increase dietary intake of potassium.
  • Teach the patient how to prevent hypokalemia by maintaining an adequate dietary intake of potassium. These include fruits, fruit juices, vegetables, or potassium supplements. Bananas and dried fruits are higher in potassium than oranges and fruit juices.
  • Administer potassium chloride supplements (Table (Potassium supplements) ) orally (may take 30 minutes for onset) or IV. Use a central IV line for rapid infusion in critical conditions. Take with at least a half a glass of fluid (juice or water) because potassium is extremely irritating to the gastric and intestinal mucosa.
  • Teach patients the signs and symptoms of hypokalemia and to call the healthcare provider if any of these are experienced.

Caution: This deficit cannot be corrected rapidly. The infusion should not exceed 10 to 20 mEq per hour or the patient may experience hyperkalemia and can experience cardiac arrest. Be alert that infusions containing potassium may cause pain at the IV insertion site. If urine output is 30 mL/hour notify prescriber. Infusions should not contain more than 60 mEq/L of potassium chloride (KCl). 40 mEq/L is the preferred amount to add to 1000 mL of intravenous solution.

Warning: NEVER give potassium as an intravenous push or intravenous bolus. This will cause immediate cardiac arrest which is not reversible with Potassium supplements.


cardiopulmonary resuscitation. Potassium must be diluted in IV fluids as stated above. Don’t give potassium if the patient suffers from renal insufficiency, renal failure, or Addison’s disease. Do not give potassium if the patient has hyper-kalemia, severe dehydration, acidosis, or takes potassium-sparing diuretics. Use with caution with patients who have cardiac disorders or burns.


Sodium is the major cation in extracellular fluid found in tissue spaces and ves-sels. Sodium plays an important role in the regeneration and transmission of nerve impulses and affects water distribution inside and outside cells. It is part of the sodium/potassium pump that causes cellular activity. When it shifts into the cell, depolarization (contraction) occurs; when it shifts out of the cell, potassium goes back into the cell and repolarization (relaxation) occurs. Sodium also combines readily in the body with chloride (Cl) or bicarbonate (HCO3) to pro-mote acid-base balance (pH).

The patient receives sodium when food is absorbed in the GI tract. Typically, a patient takes in more sodium than the patient’s daily requirement. The kidneys regulate the sodium balance by retaining urine when the sodium concentration is low and excreting urine when the sodium concentration is high. Most excess sodium is excreted in urine although sodium also leaves the patient as perspira-tion and in feces.

The serum sodium level, which is the ratio of sodium to water, is the indicator of the sodium level in a patient’s body. Sodium is measured in milliequivalents per liter (mEq/L). The normal range of serum sodium is from 135 mEq/L to 145 mEq/L.

A patient’s serum sodium level moves out of the normal range when the patient is retaining too much or too little water, has a high or low concentrations of sodium, or a combination of both. A patient is hypernatremic when there is a high concentration of sodium and hyponatremic when there is a low concentration of sodium.


Hypernatremia occurs when the patient’s serum sodium is greater than 145 mEq/L.This happens for one of two reasons: The patient’s sodium concentration has increased while the volume of water remains unchanged or the patient’s water volume has decreased while the sodium concentration remains unchanged.

Regardless of what happened, the patient experiences hyperosmolality, which is a higher-than-normal concentration of sodium. This causes water to shift out of cells and into extra cellular space resulting in cellular dehydration. A patient who is alert and can drink water to quench a thirst is at less risk for hypernatremia. However, a patient whose consciousness is impaired or who cannot swallow, such as a frail elderly patient, is at risk for hypernatremia. Hypernatremia is caused by:

  • Inadequate water intake.
  • Inability of the hypothalamus gland to synthesize anti-diuretic hormone (ADH) (which the kidneys require to regulate sodium).
  • Inability of the pituitary gland to release ADH.
  • Inability of the kidneys to respond to ADH.
  • Excess sodium (such as from a hypertonic IV solution).
  • Inappropriate use of sodium-containing drugs.
  • Ingestion of excessive amounts of sodium such as seawater.

The nurse can intervene by:

  • Replacing water using an IV of 5% dextrose in water or a hypotonic saline solution as ordered.
  • Lowering the serum sodium level slowly to avoid the risk of cerebral edema (brain swelling).
  • Restricting sodium intake.
  • Monitoring patient’s weight.
  • Assessing extremities for edema (swelling).
  • Monitoring breath sounds and respiratory effort for signs of heart failure.

The nurse must be alert to recognize the signs and symptoms of hyperna-tremia. These are:

  • Agitation
  • Restlessness
  • Weakness
  • Seizures
  • Twitching
  • Coma
  • Intense thirst
  • Dry swollen tongue
  • Edematous (swollen) extremities

The nurse should educate the patient to:

  • Avoid foods rich in sodium such as canned foods, lunch meats, ham, pork, pickles, potato chips, and pretzels. Do not add salt to foods when cooking or at the table.
  • Read all labels on food products.
  • Monitor his weight if cardiac patient by weighing daily.
  • Look for signs of swollen feet (tight shoes) and hands (tight rings).
  • Notify healthcare provider if any respiratory distress occurs.


Hyponatremia occurs when the patient’s serum sodium is less than 135 mEq/L. There are two reasons why this happens: the patient has increased the volume of water while the sodium concentration remains normal or the patient losses sodium while the water volume remains normal. Hyponatremia is caused by:

  • Profuse sweating on a hot day or after running a marathon,
  • Inappropriate administration of a hypotonic IV solution (sodium loss),
  • The result of major trauma or after surgery (sodium loss),
  • Excessive ingestion of water (water gain),
  • Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH), which causes abnormal water retention (sodium loss) or Addison’s Disease,
  • Loss of sodium from the GI tract as a result of diarrhea and vomiting (sodium loss),
  • The use of potent diuretics (lose water and salt together),
  • Burns and wound drainage (sodium loss),
  • Intake of too much water caused by polydipsia (excessive thirst).

The nurse must recognize the following symptoms of hyponatremia:

  • Fatigue,
  • Headache,
  • Muscle cramps,
  • Nausea,
  • Seizures,
  • Coma.

Hyponatremia is treated by:

  • Treating the underlying cause.
  • Administering hypertonic saline solution IV such as Dextrose 5% in saline to restore the serum sodium level.
  • Replacing fluid loss with commercially available electrolytic fluids.

The nurse should monitor:

  • Vital signs,
  • Fluid intake and output,
  • Serum sodium levels,
  • Dietary sodium intake,
  • Breath sounds and signs of respiratory distress.

The nurse should educate the patient to:

  • Not drink excessive amounts of pure water on a hot day or after extreme exercise. Fluid replacement should be an electrolyte solution such as Gatorade or other commercial preparations that include sodium.
  • Monitor for signs and symptoms of hyponatremia if the patient is taking a potent diuretic such as furosemide (Lasix) or a thiazide diuretic such as hydrochlorothiazide (HydroDiuril).
  • Report any signs of respiratory distress to healthcare provider.


Calcium is found in equal proportion in intracellular fluid and extracellular fluid. It is combined with phosphate in bone and with protein (albumin) in the serum. A patient receives calcium from ingesting calcium-containing food. Calcium plays a critical role in transmission of nerve impulses, blood clotting, muscle contraction, and the formation of teeth and bone. There is also growing evidence that calcium can help with weight loss.

There are three forms of calcium in serum that can fluctuate among forms depending on changes to the serum pH and/or serum protein (albumin) levels.

  1. Free ionized form, which is the biologically active form. Half of the patient’s total calcium is in the free ionized form.
  2. Protein bound, which binds primarily with albumin.
  3. Complex form, which is where calcium is combined with phosphate, citrate, or carbonate.

The normal serum calcium ranges between 8.5 mg/dL to 10.5 mg/dL. This reflects the calcium level for all three forms of calcium. However, ionized calcium (iC) levels are sometimes reported separately (4-5 mg/dL).

There is a balance between calcium and phosphorus. As serum calcium increases, serum phosphorus decreases. Conversely, as serum calcium decreases, serum phosphorus increases. The level of calcium is regulated by the parathyroid hormone (PTH), calcitonin, and vitamin D.

Low serum calcium causes an increase in the production of PTH. PTH moves calcium out of bone and into the serum. It increases the absorption of calcium from the GI tract. PTH also increases reabsorption of calcium in the kidneys.

Calcitonin is produced by the thyroid gland. Production is increased when there is a high serum calcium level. Calcitonin reverses the action of PTH by increasing the absorption of calcium by bone, decreases calcium absorption in the GI tract, and causes an increase in urine to excrete calcium.


Table : Medications that increase and decrease serum calcium.

Dairy products are the major source of dietary calcium. Eggs, green leafy vegetables, broccoli, legumes, nuts, and whole grains provide smaller amounts. Only about 10% to 30% of the calcium in foods is actually absorbed in the body. Calcium is absorbed in the small intestine. Absorption is influenced by the amount of vitamin D available and the levels of calcium already present in the body.


Hypercalcemia is a condition when the serum calcium level is higher than 10.5 mg/dL indicating there is a higher than normal concentration of calcium. This usually produces a low serum phosphorus level. Hypercalcemia can be caused by:

  • Renal failure.
  • Immobility.
  • Cancer.
  • Hyperparathyroidism.
  • Excess intake of calcium supplements (such as in Tums and other medications to prevent and treat osteoporosis).
  • Overuse of antacids for GI disturbances.
  • Prolonged diarrhea.
  • Excessive use of diuretics.

The nurse should be alert to identify the following signs and symptoms of hypercalcemia:

  • Patients with mild hypercalcemia may have no signs and symptoms
  • Nausea,
  • Vomiting,
  • Constipation,
  • Anorexia,
  • Abdominal pain,
  • Polyuria (frequent urination),
  • Polydipsia (extreme thirst),
  • Decreased memory,
  • Personality changes or mood swings,
  • Confusion,
  • Depressed reflexes,
  • Muscular weakness,
  • Bone pain,
  • Fractures (occur when calcium leaves the bone due to cancer, osteoporosis, and other disorders),
  • Kidney stones,
  • Hypertension,
  • Cardiac arrhythmias,
  • Coma.

Treatment is based on the calcium level. The calcium level may need to be lowered quickly because severe hypercalcemia can be life threatening. Treat the underlying cause if known.

  • If kidney function is adequate:
    • Administer isotonic saline IV to hydrate the patient.
    • Make sure the patient drinks 3000 to 4000 ml of fluid to excrete the calcium in urine.
    • Administer furosemide (Lasix) or ethcrynic acid (Edecrin) loop diuretics after adequate fluid intake is established.
  • Administer synthetic calcitonin to lower serum calcium concentration
  • Administer plicamycin (Mithracin) to increase absorption of calcium in bone.
  • Provide a low-calcium diet.
  • Make sure the patient performs weight-bearing activities.
  • Take safety measure to protect the patient who experiences neuromuscular effects.

Hemodialysis is the most effective method to lower calcium levels in severe cases when kidney function is not normal.


Hypocalcemia occurs when the serum calcium level is lower than 8.5 mg/dL indicating there is a lower than normal concentration of calcium. This usually produces a high serum phosphorus level. Too little calcium intake causes calcium to leave the bone to maintain a normal calcium level. Fractures (broken bones) may occur if a calcium deficit persists because of calcium loss from the bones (demineralization).

Hypocalcemia is caused by:

  • Hypoparathyroidism.
  • Thyroid or neck surgery where the parathyroid gland is removed or injured.
  • Hypomagnesium caused by alcoholism.
  • Ingestion of phosphates.
  • Inadequate intake of dietary calcium and/or Vitamin D.

Patients who experience hypocalcemia may have the following symptoms:

  • Depression.
  • Memory loss.
  • Confusion.
  • Hallucinations.
  • Numbness and tingling in the face, around the mouth, and in the hands and feet.
  • Muscle spasms in the face, around the mouth, and in the hands and feet.
  • Hyperreflexia.
  • Ventricular tachycardia.

Patients with hypocalcemia can be treated as follows:

  • Calcium preparations can be given PO in tablet, capsule, or powder form or IV If given IV, then mix with 5% dextrose in water. Do not mix with a saline solution because sodium encourages the loss of calcium.
  • Administer parenteral calcium. Caution: tissue infiltration leads to necrosis and sloughing. Calcium increases the action of digoxin and can result in cardiac arrest. Don’t add calcium to bicarbonate or phosphorus because precipitates form.
  • Administer the following medication intravenously if ordered:
    • Calcium chloride IV 10 mL
    • Calciumgluceptate 5 mL
    • Calcium gluconate 10 mL
  • Administer the following medication PO if ordered:
    • Calcium carbonate (Os-cal, Tums, Caltrate, Megacal) 650-1500 mg tablets
    • Calcium gluconate (Kalcinate) 500-1000 mg tablets
    • Calcium lactate 325-650 mg tablets
    • Calcium citrate 950 mg tablet
  • Take safety precautions because the patient is at risk for tetany and seizures.
  • Tell the patient to refrain from alcohol and caffeine because they inhibit calcium absorption.
  • Increase dietary calcium to 1500 mg/day by eating green leafy vegetables and fresh oysters and milk products.
  • Administer vitamin D.
  • Have the patient undergo regular exercises to decrease bone loss.

Patient education should include information about dietary sources of calcium, the need to maintain physical activity to avoid bone loss, avoid overuse of antacids, and chronic use of laxatives. Patients should be taught to use fruits and fiber for improving bowel elimination. Take oral supplements with meals or after meals to increase absorption.


Magnesium is a sister cation to potassium and is higher in intracellular fluid (ICF). If there is a loss of potassium there is also a loss of magnesium. Magnesium is the coenzyme that metabolizes carbohydrates and proteins and is involved in metabolizing nucleic acids within the cell. Magnesium also has a key role in neuromuscular excitability. The patient acquires magnesium by ingesting magnesium-rich food, where it is absorbed in the GI tract and then excreted in urine.

There is a close relationship between magnesium, potassium, and calcium. PTH (see calcium), which regulates calcium, also influences the magnesium balance. Typically, you’ll assess serum magnesium, calcium, and potassium together. The normal serum magnesium level is between 1.5 mEq/L and 2.5 mEq/L.


Hypermagnesemia is a condition experienced by a patient whose serum magnesium level is greater than 2.5 mEq/L. The major cause of hypermagnesia is an excessive intake of magnesium salts in laxatives such as magnesium sulfate, milk of magnesia, and magnesium citrate. Antacids such as Maalox, Mylanta, and DiGel can also cause hypermagnesemia. Patients who take lithium (antipsychotic medication) are also at risk for hypermagnesemia.

The signs and symptoms of hypermagnesemia are:

  • Lethargy.
  • Drowsiness.
  • Weakness.
  • Paralysis.
  • Cardiac (ventricular) arrhythmias.
  • Heart block.
  • Loss of deep tendon reflexes.
  • Hypotension.


Hypomagnesemia happens when the serum magnesium level is less than 1.5 mEq/L. This can be caused by long-term administration of saline infusions which can result in the loss of magnesium and calcium. Diuretics, certain antibiotics, laxatives, and steroids are drug groups that promote magnesium loss. Hypomagnesemia also enhances the action of digitalis and can cause digitalis toxicity.

Patients who have hypomagnesemia may exhibit no signs and symptoms until the serum level approaches 1.0 mEq/L. Signs of severe hypomagnesemia include tetany-like symptoms caused by hyperexcitability (tremors, twitching of the face), ventricular tachycardia that leads to ventricular fibrillation, and hypertension.

Treatment for hypomagnesemia includes:

  • Administering intravenous magnesium sulfate in solution slowly. Use an infusion pump to prevent rapid infusion that might result in cardiac arrest.
  • Monitoring signs of magnesium toxicity such as hot flushed skin, anxiety, lethargy, hypotension and laryngeal stridor.
  • Monitoring EKG and pulse.
  • Taking safety precautions for patients who are at risk for seizures and mental confusion.
  • Increasing the dietary sources of magnesium including nuts, whole grains, cornmeal, spinach, bananas, and oranges.

Keep calcium gluconate available for emergency reversal of hypermagnesemia as a result of overcorrecting hypomagnesemia.


Phosphate is the primary anion inside the cell and plays a key role in the function of red blood cells, muscles, and the nervous system. Phosphate is also involved the acid-base buffering and is involved with metabolizing carbohydrates, proteins, and fats. Most of the body’s phosphate (about 85%) is found in bones. The rest of it is stored in tissues throughout the body.

Phosphorus is acquired by eating phosphorus-rich foods. Phosphorus is absorbed in the GI tract and excreted in urine and a small amount in feces. It is converted to phosphate in the body.

Both phosphate and calcium levels are regulated by parathyroid hormone (PTH). The amount of phosphate in the blood effects the level of calcium in the blood. Both levels are usually measured at the same time. As the serum calcium concentration increases, the concentration of serum phosphorus decreases and conversely as serum phosphorus increases, serum calcium decreases. The nor¬mal range of serum phosphorus is between 2.5 mg/dL and 4.5 mg/dL.

The kidneys regulate the amount of phosphate in the blood. Abnormally high levels of serum phosphate are usually caused by kidney malfunction.


Hyperphosphatemia is the condition exhibited by a patient whose serum phosphate is greater than 4.5 mg/dL, which is caused by:

  • Kidney disease.
  • Under active parathyroid glands.
  • Acromegaly.
  • Rhabdomyolysis.
  • Healing fractures.
  • Untreated diabetic ketoacidosis.
  • Certain bone diseases.
  • Excessive ingestion of phosphate-containing laxatives.
  • Excessive drinking of milk.
  • Chemotherapy for neoplastic disease.
  • Excessive intake of vitamin D.
  • Decrease in magnesium levels as in alcoholism.
  • Increased phosphate levels during the last trimester of pregnancy.

Unlike hyperkalemia and hypermagnesemia, acute hyperphosphatemia causes few sudden problems. The major effect is to cause hypocalcemia and tetany if serum phosphate rises too rapidly. Calcium can be deposited in the tissues in hyperphosphatemia.

The treatment for acute hyperphosphatemia is administration of phosphate binding salts, calcium, magnesium, and aluminum although aluminum is avoided in renal failure.

Patients who have hyperphosphatemia show the following signs and symptoms:

  • Muscle problems.
  • Hyperreflexia.
  • Soft tissue calcification.
  • Nausea.
  • Vomiting.
  • Hypocalcemia.
  • Tachycardia.
  • Anorexia.
  • Tetany.

Treatment for hyperphosphatemia can include:

  • Restricting foods and drinks (carbonated soda) high in phosphate.
  • Treating the underlying cause.
  • Institute seizure precautions.
  • Administering sevelamer (Renagel).
  • Administering calcium supplements.


Hypophosphatemia occurs in a patient’s whose serum phosphate is less than 2.5 mg/dL and is caused by:

  • Inadequate intake.
  • Diuresis.
  • Dialysis.
  • Alcoholism.
  • Steroids.
  • Overuse of phosphate-binding antacids.

The nurse should monitor the patient for the following signs and symptoms of hypophosphatemia:

  • Bone and muscle pain.
  • Muscle weakness.
  • Rhabdomyolysis.
  • Confusion.
  • Osteomalacia.
  • Coma.

Hypophosphatemia can be treated by:

  • Administering phosphate supplements such as Neutra-Phos PO.
  • Administering sodium phosphate IV.
  • Administering potassium phosphate IV.

Nursing interventions should include:

  • Assessing vital signs.
  • Assessing changes in metal status.
  • Institute seizure precautions.
  • Monitor blood levels.

All rights reserved © 2020 Wisdom IT Services India Pvt. Ltd DMCA.com Protection Status

Pharmacology Topics