PHOSPHOROUS IMBALANCE
PREPARED BY :MS ALIYA MAQSOOD
NURSING LECTURER
FUNCTION
Phosphorus is a critical constituent of all the body’s tissues.
It is essential to the:
Function of muscle and red blood cells
Formation of adenosine triphosphate (ATP) and of 2,3 diphosphoglycerate
Facilitates release of oxygen from hemoglobin
Maintenance of acid–base balance, as well as the nervous system
Intermediary metabolism of carbohydrate, protein, and fat.
FUNCTION
It provides structural support to bones and teeth.
Phosphorus is the primary anion of the ICF.
About 85% of phosphorus is located in bones and teeth, 14% in soft tissue, and
less than 1% in the ECF.
The normal serum phosphorus level is 2.5 to 4.5 mg/dL (0.8 to 1.45 mmol/L)
in adults.
PHOSPHORUS DEFICIT (HYPOPHOSPHATEMIA)
• Hypophosphatemia is indicated by a value below 2.5 mg/dL (0.8 mmol/L).
Causes:
Administration of calories to patients with severe protein–calorie malnutrition
Overzealous intake or administration of simple carbohydrates
Patients with anorexia nervosa
Alcoholism
Elderly debilitated patients who are unable to eat
CAUSES
Heat stroke
Prolonged intense hyperventilation
Alcohol withdrawal
Poor dietary intake
Diabetic ketoacidosis
Respiratory alkalosis
CAUSES
Hepatic encephalopathy
Major thermal burns
Low magnesium levels
Low potassium levels
Hyperparathyroidism related to increased urinary losses of phosphorus contribute to
hypophosphatemia.
Acute volume expansion
CAUSES
Osmotic diuresis
Use of carbonic anhydrase inhibitors (acetazolamide)
Respiratory alkalosis can cause a decrease in phosphorus because of an intracellular shift of phosphorus.
Excess phosphorus binding by antacids may decrease the phosphorus.
Chronic diarrhea or through severe potassium restriction.
Vitamin D regulates intestinal ion absorption; therefore, a deficiency of vitamin D may cause de creased
calcium and phosphorus levels, which may lead to osteomalacia (softened, brittle bones).
CLINICAL MANIFESTATIONS:
Irritability
Fatigue
Apprehension
Weakness
Numbness
Paresthesias
CLINICAL MANIFESTATIONS
Dysarthria
Dysphagia
Diplopia
Confusion
Seizures
Coma
CLINICAL MANIFESTATIONS
Hypoxia leads to an increase in respiratory rate and respiratory alkalosis, causing
phosphorus to move into the cells and potentiating hypophosphatemia.
Hypophosphatemia may predispose a person to infection.
Muscle damage may develop as the ATP level in the muscle tissue declines.
Clinical manifestations are muscle weakness, which may be subtle or profound and may
affect any muscle group; muscle pain; and at times acute rhabdomyolysis (breakdown of
skeletal muscle)
CLINICAL MANIFESTATIONS
Weakness of respiratory muscles may greatly impair ventilation.
Hypophosphatemia also may predispose a per son to insulin resistance and thus
hyperglycemia.
Chronic loss of phosphorus can cause bruising and bleeding from platelet dysfunction.
ASSESSMENT AND DIAGNOSTIC FINDINGS
On laboratory analysis, the serum phosphorus level is less than 2.5 mg/dL (0.80 mmol/L) in adults.
When reviewing laboratory results, the nurse should keep in mind that glucose or insulin
administration causes a slight decrease in the serum phosphorus level.
PTH levels are increased in hyper parathyroidism.
Serum magnesium may decrease due to increased urinary excretion of magnesium.
Alkaline phosphatase is increased with osteoblastic activity.
X-rays may show skeletal changes of osteomalacia or rickets.
MEDICAL MANAGEMENT:
Prevention of hypophosphatemia is the goal.
In patients at risk for hypophosphatemia, serum phosphate levels should be closely
monitored and correction initiated before deficits become severe.
Adequate amounts of phosphorus should be added to parenteral solutions, and attention
should be paid to the phosphorus levels in enteral feeding solutions.
Severe hypophosphatemia is dangerous and requires prompt attention.
MEDICAL MANAGEMENT
Aggressive IV phosphorus correction is usually limited to the patient whose serum
phosphorus levels decrease to less than 1 mg/dL (0.3 mmol/L) and whose GI tract is not
functioning.
Possible dangers of IV administration of phosphorus include tetany from hypocalcemia
and calcifications in tissues (blood vessels, heart, lung, kidney, eyes) from
hyperphosphatemia.
IV preparations of phosphorus are available as sodium or potassium phosphate.
MEDICAL MANAGEMENT
The rate of phosphorus administration should not exceed 10 mEq/h, and the site should
be carefully monitored because tissue sloughing and necrosis can occur with infiltration.
In less acute situations, oral phosphorus replacement is usually adequate.
NURSING MANAGEMENT:
The nurse identifies patients who are at risk for hypophosphatemia and monitors them.
Because malnourished patients receiving parenteral nutrition are at risk when calories
are introduced too aggressively, preventive measures involve gradually introducing the
solution to avoid rapid shifts of phosphorus into the cells.
For patients with documented hypophosphatemia, careful attention is given to
preventing infection, because hypophosphatemia may alter the granulocytes.
NURSING MANAGEMENT
In patients requiring correction of phosphorus losses, the nurse frequently monitors
serum phosphorus levels and documents and reports early signs of hypophosphatemia
(apprehension, confusion, change in level of consciousness).
If the patient experiences mild hypophosphatemia, foods such as milk and milk
products, organ meats, nuts, fish, poultry, and whole grains should be encouraged.
• With moderate hypophosphatemia, supplements such as Neutra-Phos capsules (250 mg
phosphorus/capsule; 7 mEq sodium and potassium), K-Phos (250 mg phosphorus/tablet;
14 mEq potas sium), and Fleet’s Phospho-Soda (815 mg phosphorus/5 mL) may be
prescribed.
PHOSPHORUS EXCESS (HYPERPHOSPHATEMIA)
• Hyperphosphatemia is a serum phosphorus level that exceeds 4.5 mg/dL (1.45 mmol/L) in
adults.
Causes:
Renal failure
Increased intake
Decreased output
Shift from the intracellular to extracellular space
CAUSES
Administration of total parenteral nutrition
Chemotherapy for neoplastic disease
Hypoparathyroidism
Metabolic or respiratory acidosis
Diabetic ketoacidosis
CAUSES
Acute hemolysis
High phosphate intake
Profound muscle necrosis
Increased phosphorus absorption may also lead to this phosphorus imbalance.
Excessive vitamin D intake
COMPLICATIONS
Metastatic calcification (soft tissue, joints, and arteries)
CLINICAL MANIFESTATIONS
Tetany (high serum phosphorus level tends to cause a low serum calcium concentration)
Tingling sensations in the fingertips and around the mouth.
Anorexia
Nausea
Vomiting
Bone
CLINICAL MANIFESTATIONS:
Joint pain
Muscle weakness
Hyperreflexia
Tachycardia may occur
Soft-tissue calcification, which occurs mainly in patients with a reduced glomerular filtration rate.
Precipitation of calcium phosphate in nonosseous sites
ASSESSMENT AND DIAGNOSTIC FINDINGS:
On laboratory analysis, the serum phosphorus level exceeds 4.5 mg/dL (1.5 mmol/L) in adults.
The serum calcium level is useful also for diagnosing the primary disorder and assessing the
effects of treatments.
X-rays may show skeletal changes with abnormal bone development.
PTH levels are decreased in hypoparathyroidism.
BUN and creatinine levels are used to assess renal function.
MEDICAL MANANGEMENT:
When possible, treatment is directed at the underlying disorder.
For example, hyperphosphatemia may be related to volume depletion or respiratory or
metabolic acidosis. In renal failure, elevated PTH production contributes to a high
phosphorus level and bone disease.
Measures to decrease the serum phosphate level and bind phosphorus in the GI tract of
these patients include vitamin D preparations, such as cal citriol, which is available in
both oral (Rocaltrol) and par enteral (Calcijex, paricalcitol [Zemplar]) forms.
MEDICAL MANANGEMENT
IV administration of calcitriol does not increase the serum calcium unless its dose is
excessive, thus permitting more aggressive treatment of hyperphosphatemia with calcium-
binding antacids (calcium carbonate or calcium citrate).
Administration of Amphojel with meals is effective but can cause bone and central nervous
system toxicity with long-term use.
Restriction of dietary phosphate, forced diuresis with a loop diuretic, volume replacement
with saline, and dialysis may also lower phosphorus.
MEDICAL MANAGEMENT
• Restriction of dietary phosphate, forced diuresis with a loop diuretic, volume replacement
with saline, and dialysis may also lower phosphorus.
• Surgery may be indicated for removal of large calcium and phosphorus deposits.
NURSING MANAGEMENT
The nurse monitors patients at risk for hyperphosphatemia.
If a low-phosphorus diet is prescribed, the patient is instructed to avoid phosphorus-rich
foods such as hard cheeses, cream, nuts, meats, whole-grain cereals, dried fruits, dried
vegetables, kidneys, sardines, sweetbreads, and foods made with milk.
• When appropriate, the nurse instructs the patient to avoid phosphate-containing sub
stances such as laxatives and enemas.
NURSING MANAGEMENT
• The nurse also teaches the patient to recognize the signs of impending hypocalcemia and
to monitor for changes in urine output.
REFERENCES
• Brunner and Suddarth’s Text book of medical surgical nursing
