For some reason every patient that comes in through our doors gets their phosphate measured on arrival (and troponin and d-dimer but that's another story). We seem to admit many patients for IV phosphate replacement - which seems wrong to me, as I remember an endocrinologist telling me that phosphate levels vary on a day to day basis.
Like everything else biochemical, phosphate metabolism is very complicated. Measured phosphate levels do not accurately reflect body phosphate levels, but critically ill patients are more likely to have low phosphate levels. Low levels can also follow glucose overload and trauma. Many of our patients do have low phosphate levels - 20% to 80% of patients who present to the ED with alcoholic emergencies,
diabetic ketoacidosis (DKA), and sepsis are hypophosphataemic.
Increases in PTH cause an increase in phosphate and calcium release from bone, but
increase excretion in the kidney by inhibiting reabsorption in the proximal
Increases absorption of Ca2+ and phosphate
Hypophosphataemia often follows glucose overload and trauma.
Extreme hyperventilation in normal subjects can lower serum phosphate concentrations to below 1.0 mg/dL (0.32 mmol/L), and it is probably the most common cause of marked hypophosphatemia in hospitalized patients.
Signs and Symptoms
Low phosphate levels are normally asymptomatic.
It can cause weakness but whether this is due to the cause of the low phosphate levels or the low phosphate level itself is not known. You should be suspicious of the potential presence of hypophosphataemia in conditions that commonly cause hypophosphataemia - poor nutrition, antacid use, copd, asthma, bone pain or fractures, burns, treatment of DKA in ICU.
Severe acute hypophosphatemia can have a variety of signs, including disorientation, seizures, focal neurologic findings, evidence of heart failure, and muscle pain.
Diagnosis is biochemical:
MILD – 0.65-0.8
MODERATE – 0.32-0.65
SEVERE – actions on intestine, kidneys and bone
Treatment is typically directed at correcting the underlying disease rather than administering phosphate. I can't find any clear guidelines on when to replace phosphate - but generally it should be replaced if the level is very low, or causing symptoms (what ever these may be).
One site recommends that phosphate therapy is started in the ED for serum levels between 1.0 to 1.5
mg/dL, particularly in patients with chronic disease because these patients are at risk for progressing to severe hypophosphatemia. This can be safely accomplished by oral administration.
So does this help me when I get low phosphate levels? I think I'll just have to look hard for a cause (normally apparent) and treat the cause not the biochemistry. Long term...lets stop measuring it?