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SOURCE

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Source: Pai AB. Disorders of calcium and phosphorus homeostasis. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach, 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146061894. Accessed March 31, 2017.

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DEFINITION

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  • Serum phosphorus concentrations <2.4 mg/dL (<0.78 mmol/L)

    • Mild to moderate: 1–2 mg/dL (0.32–0.65 mmol/L)

    • Severe: <1 mg/dL (0.32 mmol/L)

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ETIOLOGY

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  • Result of decreased gastrointestinal (GI) absorption, reduced tubular reabsorption, extracellular to intracellular redistribution, or other conditions.

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PATHOPHYSIOLOGY

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  • Decreased GI absorption is seen with use of oral phosphate-binding agents and with hyperparathyroidism (decreased absorption of dietary phosphorus).

  • Reduced tubular absorption occurs with:

    • Hyperparathyroidism: elevated parathyroid hormone (PTH) leads to increase in serum calcium and decrease in serum phosphate concentrations.

    • Burn patients experience marked diuretic phase associated with impressive renal loss of phosphate.

  • Extracellular to intracellular phosphate shifts occur with:

    • Severe and prolonged respiratory alkalosis.

    • Treatment of diabetic ketoacidosis.

    • Drug therapy (eg, insulin, dextrose solutions, glucagons)

    • Alcohol withdrawal.

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EPIDEMIOLOGY

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  • Screening on admission to hospital: 1–3%

  • Hospitalized critically ill patients: 18–28%

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PREVENTION

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  • Routine addition of phosphate in concentrations of 12–15 mmol/L to parenteral nutrition important to prevent severe hypophosphatemia.

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RISK FACTORS

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  • Chronic use of phosphate-binding agents (eg, chronic kidney disease [CKD])

  • Peptic ulcer disease.

  • Hyperparathyroidism.

  • Alcoholism.

  • Diabetic ketoacidosis.

  • Parenteral nutrition.

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CLINICAL PRESENTATION

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  • Clinical manifestations depend on chronicity and severity of phosphate depletion.

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SIGNS AND SYMPTOMS
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  • Symptomatic hypophosphatemia is not evident until serum phosphate <1 mg/dL (<0.32 mmol/L).

  • Severe hypophosphatemia has diverse clinical manifestations that affect many organ systems.

  • Neurologic symptoms include:

    • Irritability.

    • Apprehension.

    • Weakness.

    • Numbness.

    • Paresthesias.

    • Dysarthria.

    • Confusion.

    • Obtundation.

    • Seizures.

    • Coma.

  • Skeletal muscle dysfunction:

    • Myalgia.

    • Bone pain.

    • Weakness.

    • Potentially fatal rhabdomyolysis.

  • Bone:

    • Osteopenia and osteomalacia with chronic hypophosphatemia due to enhanced osteoclastic resorption.

  • Cardiopulmonary:

    • Respiratory muscle weakness and diaphragmatic contractile dysfunction can cause acute respiratory failure.

    • Congestive cardiomyopathy.

    • Arrhythmias.

  • Hematologic:

    • Hemolysis.

    • Dysfunctional white blood cells leading to increased risk of infection.

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DIAGNOSIS

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MEANS OF CONFIRMATION AND DIAGNOSIS
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  • Serum phosphorus concentrations <2.4 mg/dL (<0.78 mmol/L)

  • Symptoms are not evident until serum phosphate <1 mg/dL (<0.32 mmol/L).

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LABORATORY TESTS
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  • Metabolic panel.

    • Serum phosphate.

    • Serum calcium.

    • Serum magnesium.

    • Serum potassium.

  • Parathyroid hormone.

  • Urinalysis.

    • 24-hour urine collection.

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DIFFERENTIAL DIAGNOSIS
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  • Dilated cardiomyopathy.

  • Encephalopathy.

  • Myopathies.

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DESIRED OUTCOMES

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  • Reverse signs and symptoms.

  • Normalize serum phosphate concentrations.

  • Manage underlying conditions.

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TREATMENT: GENERAL APPROACH

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  • Estimation of total body phosphate deficit difficult because phosphate is an intracellular electrolyte.

  • Rate of infusion and initial dose of IV phosphate based on:

    • Severity of hypophosphatemia.

    • Presence of symptoms.

    • Comorbid conditions.

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TREATMENT: PHARMACOLOGIC THERAPY

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  • Asymptomatic patients ...

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