Phosphorus is one of the primary intracellular ions in the body. It is found as both organic phosphorus and inorganic phosphorus salts. Phosphate plays a critical role in all of the body’s tissues. It is an important structural element in the bones and is essential to the function of muscle, red blood cells, and the nervous system. It is responsible for bone growth and interacts with hemoglobin in the red blood cells, thus promoting oxygen release to the body’s tissues. Phosphate is responsible for promotion of white blood cell phagocytic action and is important in platelet structure and function. It also acts as a buffering agent for urine. In one of its most important roles, phosphate is critical for the production of adenosine triphosphate (ATP), the chief energy source of the body. Approximately 85% of body phosphorus is in bone, and most of the remainder is intracellular; only 1% is in the extracellular fluid.
Normal serum phosphate levels are 2.5 to 4.5 mg/dL, whereas intracellular phosphorus levels are as high as 300 mg/dL. Hyperphosphatemia occurs when serum phosphorus levels exceed4.5 mg/dL. It is rare in the general population, but in patients with renal insufficiency or acute or chronic renal failure, the rate of hyperphosphatemia is approximately 70%. Phosphorus is absorbed primarily in the jejunum from foods such as red meats, fish, poultry, eggs, and milk products. Phosphate is regulated by the kidneys; 90% of phosphate excretion occurs by the renal route and 10% by the fecal route. Phosphate is also regulated by vitamin D and by parathyroid hormone. Phosphorus levels are inversely related to calcium levels.
The primary cause of hyperphosphatemia is decreased phosphorus excretion because of renal insufficiency or renal failure (acute or chronic). Decreased phosphate excretion also occurs with hypoparathyroidism. Decreased parathyroid activity leads to decreased calcium concentration and increased phosphorus concentration. Increased serum phosphorus absorption may also occur with increased intake of vitamin D or excessive quantities of milk. An increased intake of phosphorus or phosphorus-containing medications, such as enemas, laxatives, or antacids, can cause substantial absorption of phosphorus. Blood transfusions may also cause increased levels of phosphorus because phosphate leaks from the blood cells during storage. Phosphates may be released in excessive quantities in patients who are receiving chemotherapy for neoplastic diseases. Muscle necrosis because of trauma, viral infections, or heat stroke may also cause hyperphosphatemia because muscle tissues store the bulk of soft tissue phosphates.
Nursing care plan assessment and physical examination
Generally, patients with increased serum phosphorus levels exhibit signs and symptoms associated with hypocalcemia. Ask about a current history of chronic laxative or enema use, excess antacid use, and increased intake of foods containing large amounts of phosphorus (dried beans and peas, eggs, fish, meats, milk, nuts). Note if the patient has been admitted for massive burns or trauma, acute pancreatitis, acute or chronic renal failure, neoplastic disorders, or hypoparathyroidism.
Tetany, a condition that leads to increased neural excitability, may develop. Determine if the patient has experienced tingling in the fingertips or around the mouth. As tetany progresses, tingling may progress up the limbs and around the face and increase in intensity from tingling to numbness followed by pain accompanied by muscle spasm. Tetany is more common in patients who have taken an increased phosphorus load by diet or through medication. It is less likely in the renal patient because calcium ionization is increased in the presence of acidosis.
An elevated serum phosphorus level causes few signs or symptoms. Long-term consequences may involve soft tissue calcification for the patient with chronic renal failure resulting from precipitation of calcium phosphates in nonosseous sites, often the kidney, liver, and lungs. Other nonosseous sites may include arteries, joints, skin, or the corneas. Tetany may account for the majority of signs and symptoms because of hypocalcemia. Check for Trousseau’s (development of carpal spasm when a blood pressure cuff is inflated above systolic pressure for 3 minutes) and Chvostek’s (twitching facial muscles when the facial nerve is tapped anterior to the ear) signs.
Hyperphosphatemia is most often associated with other chronic problems, such as renal failure, hypoparathyroidism, or chemotherapy for neoplastic diseases. Assess the patient’s ability to cope with a serious disease and evaluate the patient’s social network for available support and coping abilities.
Nursing care plan primary nursing diagnosis: Alteration in nutrition: More than body requirements related to increased vitamin D or phosphorus intake.
Nursing care plan intervention and treatment plan
Medical treatment is aimed at managing the underlying disease process. If the hyperphosphatemia is caused by excessive phosphate administration in medications, elimination or substitution of the products remedies the problem. In some cases, pharmacologic agents, such as aluminum hydroxide, are used. In some instances, hemodialysis is needed to control the excess phosphate levels. Because hyperphosphatemia can impair kidney function, the physician monitors the patient’s renal function carefully.
Adequate levels of phosphorus are easily maintained by a normal diet because phosphorus is abundant in many foods, including red meat, poultry, eggs, vegetables, hard cheese, cream, nuts, cereals such as bran or oatmeal, dried fruits, and desserts made with milk. These foods may need to be restricted in the diet when patients have increased levels of phosphorus because of chronic diseases. Because the most common dietary factor causing hyperphosphatemia is vitamin D, it is often temporarily eliminated from the diet. A referral to a dietitian can help the patient with menu alternatives.
Identify patients at risk for hyperphosphatemia. If those patients develop any signs of tetany (tingling sensations, numbness, or muscle spasms and cramps), notify the physician immediately because airway compromise from laryngospasm is a potential complication.
Teach patients at risk for phosphorus imbalances to use care in choosing over-the-counter medications such as antacids, laxatives, and enemas. Patients should learn to read medication ingredients and check with the healthcare provider about any questions regarding the phosphorus content of medications. Make sure that the patient understands the mechanism of action of phosphate binders. Stress the need to take phosphate binders with or after meals to maximize their effectiveness. Explain that phosphate-binding medications may lead to constipation. Encourage the patient to use bulk-building supplements or stool softeners if constipation occurs.
Nursing care plan discharge and home health care guidelines
Teach the patient to avoid the use of over-the-counter medications that contain phosphorus, such as certain enemas, antacids, or laxatives. Instruct the patient to avoid foods high in phosphorus and vitamin D. Teach the patient to recognize signs of low calcium. Notify the patient of the next appointment with the healthcare provider.
No comments:
Post a Comment