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Hypophosphatemia occurs when the serum phosphorus level falls below 2.5mg/dl.


Hypophosphatemia results from several underlying mechanism that include:-

Respiratory alkalosis, one of the most common causes of hypophosphatemia, can stem from a number of conditions that produce hyperventilation, including: Acute salicylate poisoning Alcohol withdrawal Anxiety Diabetic ketoacidosis Heat stroke Pain Sepsis

Hyperglycemia an elevated serum glucose level, causes the release of insulin, which transports glucose and phosphorus into the cells. The same effect may occur in patient with diabetes who are receiving insulin, or in significantly malnourished patients(such as older adults, debilitated patients or alcoholics) or patients with anorexia nervosa

The following mal absorption syndromes are common causes of impaired intestinal absorption of phosphorus:Chronic diarrhea of laxative abuse Inadequate vitamin D intake Prolonged or excessive use of phosphorus binding antacids or sucrayate Starvation

Diuretic use is the most common cause of phosphorus loss through the kidneys. DKA is the second most common cause of hypophosphatemia in diabetic patients who have poorly controlled blood glucose levels. High glucose levels causes an osmotic diuresis and significant loss of phosphorus from the kidneys results from the fluid losses. Extensive burns also causes hypophosphatemia.


Mild to moderate hypophosphatemia typically produces no symptoms. Noticeable effects of hypophosphatemia usually occurs only on severe cases. Signs and symptoms include: Altered platelet function, resulting in bruising and bleeding Anorexia Apprehension Cardiomyopathy Chest pain Confusion Decreased cardiac contractility leading to hypotension and a low cardiac output Diplopia Dysphagia Hemolytic anemia Irritability Loss of bone density Malaise Memory loss Muscle destruction Muscle weakness

Myalgia Osteomalacia, bone pain and fractures Paresthesia Seizure or coma Slurred speech Weakened hand grasp


1. 2. 3. 4. Abnormal electrolytes(decreased magnesium levels and increased calcium levels) Elevated creatine kinase level with rhabdomyolysis Serum phosphorus level less than 2.5mg/dl X-ray studies reveals skeletal changes typical of osteomalacia or bone fracture

Treatment varies with the severity and cause of hypophosphatemia. It includes treating the underlying cause and correcting the imbalance with phosphorus replacement and a high phosphorus diet. The route of replacement therapy depends on the severity of the imbalance. Treatment for mild to moderate hypophosphatemia includes a diet high in phosphorus-rich foods, such as eggs, nuts, whole grains, meat, fish, poultry and milk products. If calcium is contraindicated or the patient cant tolerate milk, oral phosphorus supplements should be used. Oral supplements includes Neutra-phos and Neutra-phos-K and can be used for moderate hypophosphatemia. If treatment doesnt raise the phosphorus levels, determine what factors might be preventing . For the patients with severe hypophosphatemia or a nonfunctioning GI tract, IV phosphorus replacement is the recommended choice. Potassium phosphate should be given slowly. Adverse effects of IV replacement include hyperphosphatemia and hypocalcemia.

1. Monitor vital signs. Hypophosphatemia can lead to respiratory failure, low cardiac output, confusion, seizures or coma 2. Determine the patients level of consciousness and neurologic status each time you check his vitals 3. If the patient has severe hypophosphatemia monitor the rate and depth of respiration. Report signs and symptoms of hypoxia, such as confusion, restlessness, increased respiratory rate and in later stages, cyanosis.

4. Monitor the patient for evidence of heart failure related to reduced mycocardial functioning. Evidence include crackles, shortness of breath, decreased blood pressure and elevated heart rate 5. Check the patients temperature at least every 4 hours. Follow strict sterile technique in changing dressing and report signs of infection 6. Monitor patient for evidence of decreasing muscle strength, such as weak hand grasps or slurred speech 7. Give prescribed phosphorus supplements 8. Maintain a patent IV line as ordered. Infuse phosphorus solutions slowly using an infusion device to control the rate 9. Give an analgesic if ordered 10. Make sure the patient maintains bed rest. If ordered for his own safety keep the bed in its lowest position with wheels locked and side rails raised 11. Orient the patient as needed. keep clocks, calendars, and familiar personal objects within the sight 12. Inform the patient and his family that confusion caused by low phosphorus level is only temporary and will most likely decrease with therapy 13. Record the patients fluid intake and output 14. Monitor serum electrolyte levels, especially calcium and phosphorus level 15. Assist the patient with ambutation and activities of daily living

Reinforce teaching and evaluate the patients understanding of : 1. 2. 3. 4. 5. 6. 7. The nature of the condition and its causes Drug ordered The need to consult with a dietitian The need for high phosphorus diet and avoidance of alcohol The avoidance of antacids that contains phosphorus Warning signs and symptoms Maintaining follow up.

Hyperphosphatemia occur when the serum phosphate level exceeds 4.5mg/dl.


Hyperphosphatemia results from several underlying mechanism that include:-


Renal excretion of phosphorus normally equals that which the GI tract absorbs daily. Hyperphosphatemia usually results from the kidneys inability to excrete phosphorus. This occurs when the glomerular filtration rate begins to drop below 30ml/minute. Serum calcium, phosphorus and parathyroid hormone levels are used in the diagnosis of chronic renal failure and should be measured in all patients whose GFR is 60ml/minute or less.

A risk after thyroid or parathyroid surgery, hypoparathyroidism impairs synthesis of PTH. When less PTH is synthesized, less phosphorus is excreted by the kidneys, resulting in elevated serum phosphorus levels.

Several conditions can cause phosphorus to shift from the intracellular fluid to the extracellular fluid. Acid base imbalance, such as respiratory acidosis and DKA, are common examples. Any condition that causes destruction of the bodys cell can result in a shifting of phosphorus.


Increased intake of phosphorus can result from excessive phosphorus supplement use or use of laxatives and enemas that contain phosphorus such as Fleet enemas. Excessive intake of Vitamin D can result in increased absorption of phosphorus and lead to an elevated serum phosphorus level.


By itself, hyperphosphatemia causes few clinical problems. However, because phosphorus and calcium levels have an inverse relationship, hyperphosphatemia may lead to hypocalcemia, which can be life threatening. Signs and symptoms of hyperphosphatemia are usually caused by the effects of hypocalcemia. Signs and symptoms of calcification:Altered bone development Anorexia Arrhythmias Cataracts and impaired vision Conjunctivitis

Corneal haziness Cramps Decreased mental status Decreased stroke volume and cardiac output Decreased urine output Delirium ECG changes, such as prolonged QT interval and ST segment Heart failure Hyper reflexia Hypotension Irregular heart rate Muscle spasm Nausea and vomiting Pain Papular eruption on the skin Positive chvosteks and trousseaus signs that may progress to tetany Seizures


Typical laboratory findings for a patient with hyperphosphatemia include:1. 2. 3. 4. 5. ECG changes characteristics of hypocalcemia Increased blood urea nitrogen and creatine level Serum calcium level below 8.5mg/dl Serum phosphorus level above 4.5mg/dl X-ray studies that may reveals skeletal changes due to osteodystrophy(defective bone development) in chronic hyperphosphatemia

An elevated serum phosphorus level may be treated with drugs and other therapeutic measures. The treatment is aimed at correcting the underlying disorder and the hypocalcemia. If patients elevated serum phosphorus level is caused by excessive phosphorus intake, the condition may be remedied by reducing intake. Therapeutic measures include reducing dietary intake of phosphorus and eliminating the use of phosphorus based laxatives and enemas. Drug therapy may help decrease absorption of phosphorus in GI system. Drug therapy may include aluminum, magnesium, or calcium gel or phosphate binding antacid. Calcium salts such as calcium carbonate and calcium acetate are widely used to bind phosphate but may cause hypercalcemia. So careful dosing is needed. Keep in mind that a mildly elevated phosphorus level may benefit a patient with renal failure. High phosphorus level allow more oxygen to move from the red blood cells to tissues, which can help prevent hypoxemia. Treatment for the underlying cause of respiratory acidosis or DKA can lower serum phosphorus level. In a patient with diabetes the administration of insulin causes phosphorus to shift back into the cell, which can result in a decrease in serum phosphorus. As a final therapeutic intervention, hemodialysis of peritoneal dialysis may be initiated if the patient has chronic renal failure.

1. Monitor vital signs, keeping in mind the signs and symptoms of hypocalcemia and notify the physician. 2. Monitor fluid intake and output. If urine output falls below 30ml/hour, immediately notify the physician 3. Monitor serum electrolyte levels, especially calcium and phosphorus. Report changes immediately. Also monitor BUN and serum creatine levels, because hyperphosphatemia can impair renal tubules when calcification occurs. 4. Keep a flow sheet of daily laboratory test results for a patient at risk. Include BUN and serum phosphorus, calcium, and creatine level as well as fluid intake and output. Keep the flow sheet on a clip board so changes can be detected immediately. 5. Give prescribed drugs. 6. Prepare the patient for possible dialysis if hyperphosphatemia is severe

Reinforce teaching and evaluate the patients understanding of : 1. 2. 3. 4. 5. 6. 7. The nature of the condition and its causes Drug ordered The need to consult with a dietitian The need to avoid high phosphorus diet The avoidance of preparations that contain phosphorus(laxatives, enemas) Warning signs and symptoms Maintaining follow up.

Hyperchloremia, an excess of chloride in extracellular fluid, occurs when serum chloride levels exceed 108meq/l.


Hyperchloremia results from several underlying mechanism that include:-


Increased intake and absorption of chloride as sodium chloride can cause hyperchloremia, especially if water is lost from the body at the same time, which causes the chloride level to rise even more. Increased chloride absorption by the bowel can occur in patients who have had anastamosis joining the ureter and intestines. Conditions that alter electrolyte and acid base balance and cause metabolic acidosis along with hyperchloremia, include dehydration , renal tubular acidosis, renal failure, respiratory alkalosis, salicylate toxicity, hyperparathyroidism, hyperaldosteronism and hypernatremia


Several drug can also contribute to hyperchloremia,. Direct ingestion of ammonium chloride or other drugs that contain chloride or cause chloride retention can lead to hyperchloremia. Ion exchange resins that contain sodium, such a kayexalate, can cause chloride to be exchanged for

potassium in the bowel. When chloride follows sodium into the blood stream, serum chloride level rise. Carnonic anhydrase inhibitors such as acetazolamide, also promote chloride retention in the body by increasing bicarbonate ion loss.


Hyperchloremia rarely produces signs and symptoms on its own. Instead the major signs and symptoms are essentially those of metabolic acidosis, including tachypnea, lethargy, weakness, diminished cognitive ability and deep, rapid respirations such as Kussmauls respirations Left untreated, acidosis can lead to arrhythmias, decreased cardiac output, a further decrease in the patients level of consciousness and even coma. Metabolic acidosis related to a high chloride level is called hyperchloremic metabolic acidosis. If a patient has an increased serum chloride level, his serum sodium level is probably high as well, which can lead to fluid retention. He may also be agitated and have dyspnea, tachycardia, hypertension, edema.


1. Serum chloride level greater than 106meq/L 2. Serum pH level less than 7.35, serum bicarbonate level less than 22meq/L, and a normal anion gap (8 to 14meq/L) suggesting metabolic acidosis 3. Serum sodium level greater than 145meq/L

Treatment for hyperchloremia includes correcting the underlying causes as well as restoring fluid, electrolyte, and acid base balance. Dehydrated patients may receive fluids to dilute the chloride and speed the excretion of chloride ions through increasing urine production. Sodium and chloride intake may also be restricted. If the patients liver function is normal, he may receive an infusion of lactated Ringers solution to convert lactate to bicarbonate in the liver and to increase the base bicarbonate level and correct acidosis. In severe hyperchloremia, IV sodium bicarbonate may be administered to raise serum bicarbonate levels. Because bicarbonate and chloride complete for sodium, IV sodium bicarbonate therapy can lead to renal excretion of chloride ions and correction of acidosis

1. Monitor vital signs, including cardiac rhythm 2. If the patient is confused, reorient him as needed and provide a safe, quiet environment to prevent injury. Teach the patients family to do the same

3. Continually check the patient, paying particular attention to neurologic, cardiac and respiratory examination 4. Look for changes in the respiratory pattern that may indicate a worsening of the acid base imbalance 5. Give IV fluids as ordered. Watch the signs of fluid overload 6. Evaluate muscle strength, and adjust activity level accordingly 7. Restrict fluids, sodium, and chloride if ordered 8. Monitor and record serum electrolyte level and arterial gas results 9. Monitor and record fluid intake and output

Reinforce teaching and evaluate the patients understanding of:1. 2. 3. 4. 5. The description of hyperchloremia and its risk factors, prevention and treatment Warning signs and symptoms and when to report them Dietary restrictions if ordered Drugs if prescribed The importance of replenishing fluids during hot weather

Hypochloremia is a deficiency of chloride in extracellular fluid. It occurs when serum chloride levels falls below 96meq/l


Hypochloremia results from several underlying mechanism that include:-


Reduced chloride intake may occur in infants being fed chloride deficient formula and in people on salt restricted diets. Patients dependent on IV fluids are also at risk if the fluids lack chloride such as a dextrose solution without electrolytes.


Excessive chloride losses can occur with prolonged vomiting, diarrhea, severe diaphoresis, gastric surgery, nasogastric suctioning and other GI tube drainage. Severe vomiting can cause a loss of hydrochloric acid from the stomach, an acid deficit in the body, and subsequent metabolic alkalosis. Patients with cystic fibrosis can also lose more chloride than normal. Any prolonged and untreated hypochloremic state can result in hypochloremic alkalosis.

People at risk for hypochloremia include children with prolonged vomiting from pyloric obstruction and those with draining fistulas and ileostomies that can cause a loss of chloride from the GI tract. Various drugs may decrease chloride, including bicarbonate, corticosteroids, laxatives and theophylline. Diuretics such as frusemide, ethacrynic acid, and hydrochlorthiazide may also cause an excessive loss of chloride because chloride ions are excreted by the kidneys with cations.

Other causes of hypochloremia include sodium and potassium deficiency or metabolic alkalosis; conditions that affect acid base or electrolyte balance, such as untreated diabetic ketoacidosis and Addisons disease; and rapid removal of ascetic fluid during paracentesis. Also patients who have heart failure may develop hypochloremia because serum chloride levels are diluted by excess fluid in the body.


Patients who have hypochloremia may have signs and symptoms of acid base and electrolyte imbalances. You may notice signs of hyponatremia, hypokalemia or metabolic alkalosis. Alkalosis results in a high pH and to compensate, respirations become slow and shallow as the body tries to retain carbon dioxide and restore the pH level to normal. The nerves also become more excitable, so watch for tetany, hyperactive deep tendon reflexes, and muscle hypertonicity. The patient may have muscle cramps, twitching and weakness and be agitated or irritable. If hypochloremia goes unrecognized, it can become life threatening. As the chloride imbalance worsens, along with other imbalances, the patient may suffer arrhythmias, seizures, coma, or respiratory arrest.


1. Serum chloride level less than 98meq/L 2. Serum pH greater than 7.45 and serum bicarbonate level greater than 26meq/L indicating metabolic alkalosis. 3. Serum sodium level less than 135meq/L indicating hyponatremia

Treatment for hypochloremia focuses on correcting the underlying cause, such as low dietary chloride intake, prolonged vomiting, or gastric suctioning. Chloride may be replaced through fluid administration or drug therapy. The patient may also require treatment for associated

metabolic alkalosis or electrolyte imbalance such as hypokalemia. If the patient doesnt respond to treatment, check for other contributing factors. Chloride may be given orally, for example, in a salty broth. If the patient cant take oral supplements, he may receive drugs or normal saline solution IV. To avoid hypernatremia, which causes a high sodium level, or to treat hypokalemia, potassium chloride may be administered IV. Treatment for associated metabolic alkalosis usually addresses the underlying causes. The underlying cause of diaphoresis, vomiting or other GI losses, or renal losses should be investigated. Rarely, metabolic alkalosis may be treated by giving ammonium chloride, an acidifying agent thats used when alkalosis is caused by chloride loss. Drug dosage depends on the severity of the alkalosis. The effects of ammonium chloride last only 3 days. After that, the kidneys begin to excrete the extra acid.

Monitor patients at risk for hypochloremia, such as those receiving diuretics therapy or NG suctioning. When caring for patient with hypochloremia take these nursing actions:1. Monitor level of consciousness, muscle strength, and movement. 2. Notify the physician if the patients condition worsens 3. Monitor and record serum electrolyte levels, especially chloride, sodium, potassium, and bicarbonate. Also check arterial blood gas result for acid base imbalance. 4. If the patient is alert and can swallow without difficulty, offer salty broth. Dont let the patient fill up on plain drinking water; this will further dilute an already low chloride level 5. Give chloride and potassium replacement as ordered 6. If giving ammonium chloride, check the patient for pain at the infusion site and adjust the rate, if needed. Because ammonium chloride is metabolized by the liver, dont give it to a patient with severe hepatic disease. 7. Use normal saline solution, not tap water, to flush the patients NG tube 8. Accurately measure and record intake and output, including the volume of vomitus and gastric contents from suction and other GI drainage tubes 9. Provide a safe environment. Help the patient ambulate and keep his personal items and call button within reach. Enact seizure precautions as needed 10. Provide a quiet environment, explain interventions, and reorient the patient as needed 11. Document all care and the patients response