Hypophosphatemia is an electrolyte disturbance in which there is an
abnormally low level of phosphate in the blood. The condition has many causes,
but is most commonly seen when malnourished patients are given large
amounts of carbohydrates, which creates a high phosphorus demand by cells,
removing phosphate from the blood. Because a decrease in phosphate in the
blood is sometimes associated with an increase in phosphate in the urine, the
terms hypophosphatemia and "phosphaturia" are occasionally used
interchangeably; however, this is improper since there exist many causes
of hypophosphatemia besides overexcretion and phosphaturia, and in
fact the most common causes of hypophosphatemia are not associated with
phosphaturia. Common causes of hypophosphatemia
Refeeding syndrome This causes a demand for phosphate in cells due to the action
of Hexokinase, an enzyme that attaches phosphate to glucose to begin metabolism
of glucose. Also, production of ATP when cells are fed and recharge their energy
supplies, requires phosphate. Respiratory alkalosis Any alkalemic
condition moves phosphate out of the blood into cells. This includes most
common respiratory alkalemia, which in turn is caused by any hyperventilation.
This phenomenon is seen because in respiratory alkalosis carbon dioxide
decreases in the extracellular space, causing intracellular CO2 to freely
diffuse out of the cell. This drop in intracellular CO2 causes a rise in
cellular pH which has a stimulating effect on glycolysis. Since the process
of glycolysis requires phosphate, the result is a massive uptake of phosphate
into metabolically active tissue from the serum. It is interesting to note,
however, that this effect is not seen in metabolic alkalosis, for in such cases
the cause of the alkalosis is increased bicarbonate rather than decreased CO2.
Bicarbonate, unlike CO2, has poor diffusion across the cellular membrane
and therefore there is little change in intracellular pH.
Alcohol abuse Alcohol impairs phosphate absorption. Alcoholics are usually also
malnourished with regard to minerals. In addition, alcohol treatment is
associated with refeeding, and the stress of alcohol withdrawal may create
respiratory alkalosis, which exacerbates hypophosphatemia.
Malabsorption This includes GI damage, and also failure to absorb phosphate due
to lack of vitamin D, or chronic use of phosphate binders such as sucralfate,
aluminum-containing antacids, and calcium-containing antacids.
Primary hypophosphatemia is the most common cause of nonnutritional rickets.
Laboratory findings include low-normal serum calcium, moderately low serum
phosphate, elevated serum alkaline phosphatase, and low serum 1,25
dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of
hyperparathyroidism. Other rarer causes include
Certain blood cancers such as lymphoma or leukemia
Hereditary causes Liver failure
Tumor-induced osteomalacia Pathophysiology
Hypophosphatemia is caused by the following three mechanisms:
Inadequate intake Increased excretion
Shift from extracellular to intracellular space and acute
respiratory alkalosis) Major signs and symptoms
Muscle dysfunction and weakness. This occurs in major muscles, but also may
manifest as: diplopia, low cardiac output, dysphagia, and respiratory
depression due to respiratory muscle weakness.
Mental status changes. This may range from irritability to gross confusion,
delirium, and coma. White cell dysfunction, causing
worsening of infections. Instability of cell membranes due to low
ATP levels: this may cause rhabdomyolysis with increased CPK, and
also hemolytic anemia. Increased affinity for oxygen in the
blood caused by decreased production of 2,3BPG.
Large pulp chambers in the teeth. Treatment
Standard intravenous preparations of potassium phosphate are available and
are routinely used in malnourished patients and alcoholics. Oral
supplementation also is useful where no intravenous treatment is available.
Historically one of the first demonstrations of this was in
concentration camp victims who died soon after being re-fed: it was observed that
those given milk had a higher survival rate than those who did not get milk.
monitoring parameters during correction with IV phosphate
Phosphorus levels should be monitored after 2 to 4 hours after each dose, also
monitor serum potassium, calcium and magnesium. Cardiac monitoring is also
advised. See also
Hyperphosphatemia Hypophosphatasia
X-linked hypophosphatemia External links
eMedicine review Tutorial - complications
Refeeding Syndrome References