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The normal plasma phosphate concentration is 2.5-4.5 mg/dL, also expressed as 0.81-1.45 mmol/liter; a factor of approximately 3 can be used for conversion between units Due to the valence varying with pH, it is less meaningful to express phosphate concentration in mEq/liter
Moderate depletion is defined as 1.0-2.0 mg/dL, and severe as <1.0 mg/dL, while severe overload is defined as >14 mg/dL
There is a mean diurnal variation in the plasma concentration of 0.6 ± 0.1 mg/dL, with the nadir at 11:00 AM, and the peak at 12:30 AM
Normal 0.8-1.45 mmol/L or 2.5-4.5 mg/dl
increased renal excretion
or redistribution of inorganic phosphate
redistribution is the most common in the critically ill
levels are inversely proportional to inflammatory cytokines
Use K Phos if K is less than 4 or Na Phos if higher
affects many different organ systems.
Although the underlying nutritional status of the patient, reflected by the serum prealbumin level, appears to impact the clinical severity, the correlation is relatively loose between serum phosphate concentrations and symptoms
Myalgias, muscle weakness, and anorexia, usually the earliest symptoms, typically occur at serum levels below 1.5 mg/dL. At phosphate levels below 0.8 mg/dL the neurologic symptoms (paresthesias, tremor, confusion, decreased deep tendon reflexes, seizures, and coma) may progressively develop. Rhabdomyolysis may occur due to structural and functional disturbances in skeletal muscle membranes, and hyperglycemia may be present due to insulin resistance. Hemolysis due to increased erythrocyte membrane rigidity, and reduced leukocyte and platelet function also may occur.
Other serious clinical disorders resulting from hypophosphatemia include ventricular tachycardia, decreased tissue oxygenation (due to high hemoglobin affinity from reduced 23DPG levels impairing O2 release), respiratory failure secondary to diaphragmatic weakness, hypotension, and congestive heart failure due to reduced cardiac contractility. These disorders can be reversed with phosphate administration, but the abnormality must be considered so that the diagnosis can be made and treatment instituted
Causes: loop diuresis, DKA, hyper-pth, malnutrition, refeeding syndrome, insulin therapy, alkalosis
associated with effects on many organ systems as well. Because the complications of hyperphosphatemia are not even as predictable as those due to phosphate depletion, phosphate levels are typically described as elevated or severely elevated. Weakness, tetany, seizures, and dysrhythmias, including polymorphic ventricular tachycardia and torsades de pointes due to prolongation of the Q-T interval, can occur with hyperphosphatemia. These effects are not caused directly by the elevated phosphate, but are instead due to the resultant hypocalcemia. The reduction in ionized calcium can be demonstrated by the steady state reaction between calcium and phosphate. Hypomagnesemia, hypernatremia, and metabolic acidosis are also associated with hyperphosphatemia.
Oral therapy is preferred over the IV route based on safety, no need for subsequent monitoring of electrolytes, and ease of administration. The plasma phosphate level peaks 1.5 h post ingestion, and typically rises 1 mg/dl for a 1g dose of phosphorous. The dosing for oral and IV therapy can be confusing due to the various preparations being either in units of mg of phosphorous or mmol of phosphate. Thirty-one milligrams of elemental phosphorous is equivalent to 1 mmol of phosphate. Treatment dosing should aim for at least 1g daily (15 mg/kg), but may initially need to be as high as 3 g daily for severe total body phosphate deficiency. Diarrhea and gastric irritation are the most common adverse effects, occurring typically in a dose-dependent manner if greater than 1 g is given. These undesirable effects can be reduced by dividing the total dose into three to four smaller daily doses. Cow’s milk is a good source of elemental phosphorous, containing 1 mg per 1cc. Alternatively, four tablets or packets of sodium phosphate (NaPO4) or potassium phosphate (KPO4) also contain 1 g. Potassium phosphate is often used for oral repletion since hypokalemia is commonly found in patients with hypophosphatemia.
For severe or symptomatic hypophosphatemia, IV repletion should be begun in the ED, with a goal serum level of 2.0 mg/dL, before patient discharge. Those patients with severe symptoms (cardiac, pulmonary, CNS), or those requiring multiple infusions due to total-body depletion, should be admitted. The phosphate should be administered in saline or dextrose solutions instead of lactated Ringers, which contains calcium and can form calcium-phosphate precipitates. Phosphate distribution varies among patients, so there are no reliable formulas for dosing based upon the phosphate deficit. Because the response for any given dose is unpredictable, it is recommended to check serum phosphate, calcium, and magnesium levels every 6 h while administering parenteral phosphate therapy. Close monitoring is necessary during IV administration for early detection of the potential complications, including “overshoot” hyperphosphatemia, hypocalcemia, and hypomagnesemia.
There are multiple suggested regimens for IV replacement. A commonly accepted therapy is 4.5 mmol/h for 3 h, up to 90 mmol in 24 h. There are weight based regimens, giving 0.08 mmol/kg over 6 h for acute hypophosphatemia (usually due to intracellular shifts) and 0.16 mmol/kg over 6 h for chronic depletion (reflecting that the total-body phosphate deficit will be more resistant to therapy). More rapid replacement regimens have been advocated for use in critically ill patients. One study found 15 mmol given over 2 h in the intensive care unit (ICU) to be safe. Another study of septic ICU patients gave 20 mmol over one hour without any significant complications. Phosphate deficit correction in this patient population was found to increase systolic blood pressure by 12% and to improve cardiac index by 22-28%, possibly through improved response to vasopressors.
Hyperphosphatemia is best managed by treating the underlying disorder, such as administering IV saline for rhabdomyolysis and tumor-lysis syndrome. Patients with chronic renal failure and mild asymptomatic hyperphosphatemia can be treated by reducing dietary phosphate intake (protein) and blocking intestinal absorption with phosphate-binding salts of aluminum, magnesium, or calcium. Aluminum-containing salts can have significant toxicity if used chronically, and caution must be used with calcium-containing salts if the calcium-phosphate product is greater than 70. Use of magnesium-containing salts may induce hypermagnesemia in patients with renal insufficiency. Hemodialysis or peritoneal dialysis can be used to effectively correct acute severe hyperphosphatemia and symptomatic hypocalcemia rapidly and safely in patients with end-stage renal disease.
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