It is diagnosed based on a blood phosphate concentration of less than 0.81 mmol/L (2.5 mg/dL).[1] When levels are below 0.32 mmol/L (1.0 mg/dL), it is deemed to be severe.[2]
Treatment depends on the underlying cause.[1] Phosphate may be given by mouth or by injection into a vein.[1] Hypophosphatemia occurs in about 2% of people within hospital and 70% of people in theintensive care unit (ICU).[1][4]
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.[citation needed]
Mental status changes – This may range from irritability to gross confusion, delirium, and coma.[citation needed]
Refeeding syndrome – This causes a demand for phosphate in cells due to the action ofhexokinase, an enzyme that attaches phosphate to glucose to begin metabolism of glucose. Also, production ofATP when cells are fed and recharge their energy supplies requires phosphate. A similar mechanism is seen in the treatment ofdiabetic ketoacidosis,[5] which can be complicated byrespiratory failure in these cases due to respiratory muscle weakness.[6][7]
Respiratory alkalosis – Any alkalemic condition moves phosphate out of the blood into cells. This includes most common respiratory alkalemia (a higher than normal blood pH from low carbon dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes). This phenomenon is seen because in respiratory alkalosis carbon dioxide (CO2) 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 onglycolysis. Since the process of glycolysis requires phosphate (the end product isadenosine triphosphate), the result is a massive uptake of phosphate into metabolically active tissue (such as muscle) from the serum. However, that this effect is not seen inmetabolic 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.[8]
Alcohol use disorder – Alcohol impairs phosphate absorption. People who excessively consume alcohol are usually also malnourished with regard to minerals. In addition, alcohol treatment is associated with refeeding, which further depletes phosphate, and the stress ofalcohol withdrawal may create respiratory alkalosis, which exacerbates hypophosphatemia (see above).[citation needed]
Malabsorption – This includes gastrointestinal damage, and also failure to absorb phosphate due to lack of vitamin D, or chronic use of phosphate binders such assucralfate, aluminum-containing antacids, and (more rarely) calcium-containing antacids.[citation needed]
Intravenous iron (usually for anemia) may cause hypophosphatemia. The loss of phosphate is predominantly the result of renal wasting.[citation needed]
Cannabinoid hyperemesis syndrome (CHS), where individuals vomit cyclically for long periods of time, has been found to cause hypophosphatemia. A report on 3 patients with CHS found each to have moderate to severe hypophosphatemia which requiredintravenous phosphate replacement. Common causes for hypophosphatemia were explored in these patients but the aetiology was not discovered.[9] However, other case reports posit that hyperventilation could be a potential cause.[10]
Hypophosphatemia is diagnosed by measuring the concentration of phosphate in the blood. Concentrations of phosphate less than 0.81 mmol/L (2.5 mg/dL) are considered diagnostic of hypophosphatemia, though additional tests may be needed to identify the underlying cause of the disorder.[12]
Standard intravenous preparations of potassium phosphate are available and are routinely used in malnourished people and people who consume excessive amounts of alcohol. Supplementation by mouth is also useful where no intravenous treatment are available. Historically one of the first demonstrations of this was in people in concentration camp who died soon after being re-fed: it was observed that those given milk (high in phosphate) had a higher survival rate than those who did not getmilk.[citation needed]
Monitoring parameters during correction with IV phosphate[13]
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.[citation needed]
