Critical Care Medicine

Hypo/hyperphosphatemia

Hypophosphatemia and hyperphosphatemia

Also known as: Low serum phosphate and high serum phosphate

Related conditions: Rhabdomyolysis, crush injury, kidney injury

1. Description of the problem

What every clinician needs to know

85% of phosphorous is present in bones and teeth, 14% is in soft tissues and 1% is in extracellular space. 60% of plasma phosphate is present in ionized forms; whereas remaining is bound to plasma proteins or other cations such as calcium, sodium and magnesium.

Normal serum phosphate levels vary with age, with values between 4.8-8.2 mg/dl in newborn to 2.7-4.7 mg/dl in older adolescents

Clinical features

Symptoms of hypophosphatemia manifest when serum phosphate levels fall below 1-1.5mg/dl: patient may have muscle weakness, lethargy, paralysis, seizures and coma. Muscle weakness can result in respiratory failure. Also present with leukocyte, platelet dysfunction and rhabdomyolysis.

Hyperphosphatemia in itself doesn't cause any symptoms other than a hypocalcemic response due to increased Ca X P product which promotes soft tissue calcification.

Key management points

Identify cause. Serum phosphate below 1.5 mg/dl or symptomatic hypophosphatemia may need IV replacement.

Hyperphosphatemia is treated by intravascular volume expansion and stopping excess intake. Dialysis may be required in patients with kidney injury.

2. Emergency Management

Hypophosphatemia: if serum phosphate is below 1.5/symptomatic patient, give 2.5-5 mg/kg IV elemental phosphate over 6 hours.

Hyperphosphatemia: intravascular volume expansion with normal saline and dialysis in acute kidney injury.

3. Diagnosis

Diagnostic criteria and tests

Hypophosphatemia is diagnosed if serum phosphate is below 2 mg/dl. Other labs to send include total serum calcium, circulating PTH and vitamin D. Hypophosphatemia should be suspected in patients with protein calorie malnutrition (infants), and disorders of the duodenum and jejunum. Drugs such as acetazolamide, cisplatin, glucocorticoids can lead to hypophosphatemia

Hyperphosphatemia is diagnosed when serum phosphate is above 4.7 mg/dl. Hypophosphatemia should be suspected in patients with acute or chronic kidney injury, in patients with crush injury or tumor lysis syndromes, and in small children who were given phosphate enemas.

Normal lab ranges

Normal serum phosphate ranges between 4.8-8.2 mg/dl (in newborns) and 2.7-4.7 mg/dl in older adolescents.

Establishing the diagnosis

Hypophosphatemia should be suspected in patients who present with seizures, lethargy, muscle weakness and respiratory depression.

Hyperphosphatemia should be suspected in patients with acute/chronic kidney injury, crush injury, rhabdomyolysis and tumor lysis syndrome.

4. Specific Treatment

First-line therapy

Hypophosphatemia: treat only if symptomatic or levels are below 1.5mg/dl.

Hyperphosphatemia can be treated with intravascular fluid hydration or dialysis in patients with kidney injury.

Drugs and dosages

For hypophosphatemia: IV elemental phosphorous 2.5-5mg/kg over 6 hours

5. Disease monitoring, follow-up and disposition

Closely follow serum levels as treatment is initiated. Monitored bed may be required.

Pathophysiology

Hypophosphatemia is usually caused by decreased dietary intake or decreased renal absorption as seen in hyperparathyroidism. It can also be seen in patients - especially premature infants - who ingest unsupplemented breast milk. Hypophosphatemia may be seen in chronically malnourished patients who are administered carbohydrate, which leads to rapid release of insulin. The insulin will stimulate uptake of phosphate, leading to symptomatic hypophosphatemia (refeeding syndrome).

Hyperphosphatemia is seen in acute or chronic kidney injury due to limitation of phosphate excretion.

Prognosis

Good provided underlying disease is treated.

Special considerations for nursing and allied health professionals.

Close monitoring of serum levels is important.

What's the evidence?

Greenbaum, LA, Berhman, RE, Kliegman, RM, Jensen, HB. "Pathophysiology of body fluids and fluid therapy". Nelson Textbook of Pediatrics. WB Saunders. 2004.

Suki, WN, Lederer, ED, Rouse, D, Brenner, BM. "Renal Transport of Calcium, Magnesium and Phosphate". Brenner and Rectors The Kidney. WB Saunders. 2000. pp. 520-74.

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