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hyperphosphatemia/hy·per·phos·pha·te·mia/ (-fos″fah-te´me-ah) an excessive amount of phosphates in the blood.
hyperphosphatemiaNephrology↑ Phosphate > 1.5 mmol/L–US: 4.5 mg/dL in blood Etiology ↑ hGH, either physiologic with growth spurts or pathologic in gigantism and acromegaly, ↓ PTH, pseudohypoparathyroidism or in renal failure
|Mean LOS:||4.6 days|
|Description:||MEDICAL: Inborn and Other Disorders of Metabolism|
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, 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, 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 exceed 4.5 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.
Hyperphosphatemia can be seen as a feature of familial endocrine abnormalities, such as familial tumoral calcinosis with hyperphosphatemia. Mutations in the GALNT3 gene cause hyperostosis with hyperphosphatemia (HHS). There is an autosomal dominantly transmitted form of hypoparathyroidism with variable expressivity that includes high phosphate with low calcium and magnesium levels.
Gender, ethnic/racial, and life span considerations
Serum levels of phosphate are normally higher (3.5 to 5.5 mg/dL) in children because of the increased rate of skeletal growth. Infants who are fed cow’s milk or formula may develop hyperphosphatemia because cow’s milk contains more phosphorus (940 mg/L) than human milk (150 mg/L). The most common cause, renal failure, occurs across the life span and in both sexes. Women have a slight but nonclinical elevation of serum phosphate levels after menopause. While hyperphosphatemia has no racial or ethnic predilection, African Americans, people of Hispanic origin, and Native Americans have a disproportionately high prevalence of renal failure, which can result in hyperphosphatemia.
Global health considerations
Experts suggest that rates of hyperphosphatemia parallel those of renal failure around the world.
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.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Serum phosphorus||2.5–4.5 mg/dL||> 4.5 mg/dL (adults); > 5.5 mg/dL (children); critical value: > 5 mg/dL in adults||Reflects phosphorus excess|
|Serum calcium||8.6–10.3 mg/dL||< 8.5 mg/dL||Reflects calcium deficit|
|Serum ionized calcium (free calcium)||4.5–5.1 mg/dL||< 4.5 mg/dL||Reflects ionized calcium (46%–50% of circulating calcium)|
Other Tests: Electrocardiogram, blood urea nitrogen, creatinine
Primary nursing diagnosis
DiagnosisAlteration in nutrition: More than body requirements related to increased vitamin D or phosphorus intake
OutcomesNutritional status: Food and fluid intake; Nutrient intake; Knowledge: Medication, Treatment regimen
InterventionsElectrolyte management: Hyperphosphatemia; Fluid balance; Electrolyte management: Hypocalcemia; Medication administration; Medication management; Surveillance
Planning and implementation
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.
|Medication or Drug Class||Dosage||Description||Rationale|
|Acetazolamide (Diamox)||250–375 mg PO/IV daily||Diuretic carbonic anhydrase inhibitor|
|Phosphate-binding agents (aluminum-containing binders are no longer prescribed because of the toxic effects of aluminum)||Varies with drug||Sevelamer hydrochloride (Renagel); lanthanum carbonate (Fosrenol); sucroferric osyhudroxide (Velphoro); calcium acetate, calcium carbonate||Cause phosphate binding in the gastrointestinal tract, thereby decreasing serum phosphate levels|
Other Drugs: Calcium supplements to prevent tetany
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 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.
Evidence-Based Practice and Health Policy
Foley, R.N., Collins, A.J., Herzog, C.A., Ishani, A., & Kalra, P.A. (2009). Serum phosphorus levels associate with coronary atherosclerosis in young adults. Journal of the American Society of Nephrology, 20(2), 397–404.
- Investigators conducted a 15-year prospective study among 3,015 healthy young adults to determine the effects of phosphorus on cardiovascular risk and found that each 0.5-mg/dL increase in phosphorus levels at baseline was associated with a 13% decreased risk of coronary artery calcification (95% CI, 0.77 to 0.99; p = 0.0332). The mean phosphorus level for the entire sample at baseline was 3.6 mg/dL (SD, ± 0.5 mg/dL; range, 1.3 to 5.7 mg/dL).
- In this sample, 3.2% had minimal coronary artery calcification, 4.8% had mild calcification, 1.1% had moderate calcification, and 0.5% had severe calcification at year 15.
- Physical response: Signs of tetany (tingling sensations, numbness, muscle spasms, or cramps)
- Phosphate levels
- Emotional response to chronic illness
Discharge and home healthcare 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.