Phosphate

• distributed in similar concentrations throughout intracellular and

extracellular fluid.90% in bone, 10% is intracellular, and <1%, in the ECF.
• free ion (55%), complexed ion (33%), and in a protein-bound form (12%).
• Control of phos concentration by altered renal excretion and redistribution
within the body compartments.
• Absorption occurs in the duodenum and jejunum and is largely unregulated.
Phos reabsorption in the kidney is primarily regulated by PTH, dietary
intake, and insulin-like growth factor.
• Phos provide the primary energy bond in ATP and creatine phosphate.
Therefore, severe phosphate depletion results in cellular energy depletion.
• Phos is an essential element of second-messenger systems, including cAMP
and phosphoinositides, and a major component of nucleic acids,
phospholipids, and cell membranes.
• As part of 2,3-DPG, phos is important for off-loading oxygen from the
hemoglobin molecule.
Hypophosphatemia
• CNS: paresthesias, myopathy, encephalopathy, delirium, seizures, and
coma.
• Hematologic: dysfunction of erythrocytes, platelets, and leukocytes.
• Muscle weakness and malaise are common.
• Respiratory muscle failure and myocardial dysfunction are potential
problems of particular concern to anesthesiologists.
• Rhabdomyolysis is a complication of severe hypophosphatemia.
• Carbohydrate-induced hypophosphatemia (the “refeeding syndrome”), and
during medical management of DKA.
• Acute alkalemia, which may reduce serum PO4, Hyperventilation to a
PaCO2 of 20 mm Hg may reduce the serum PO4
• Excessive renal loss of PO4 with hyperparathyroidism, hypomagnesemia,
hypothermia, diuretic therapy, and renal tubular defects in PO4 absorption.
• GI loss due to the use of PO4-binding antacids or to malabsorption
syndromes.
• Measurement of urinary PO4 aids in differentiation due to renal losses from
that due to excessive GI losses or redistribution of PO4 into cells
• Patients with severe or symptomatic require IV phos administration
• 15-mmol boluses (465 mg) mixed with 100 ml of 0.9% sodium chloride
and given over a 2-hour period safely repletes phosphate.
• Phosphate should be administered cautiously to hypocalcemic patients
because of the risk of precipitating more severe hypocalcemia.
Hyperphosphatemia
• clinical features relate to the hypocalcemia and ectopic calcification.
• caused by 3 basic mechanisms: inadequate renal excretion, ↑movement of
PO4 out of cells, and ↑ PO4 or vitamin D intake.
• Rapid cell lysis from chemotherapy, rhabdomyolysis, and sepsis can cause
hyperphosphatemia, especially when renal function is impaired.
• Renal failure is the most common cause of hyperphosphatemia.
• BUN, creat, GFR, and urinary PO4 are helpful in the DDx of ↑phos.
• corrected by eliminating the cause of the ↑PO4 and correcting ↓Ca
• Calcium supplementation of hypocalcemic patients should be delayed until
serum phosphate has fallen below 2.0 mmol·l–1
• The serum PO4 is ↓ by restricting intake, ↑urinary excretion with saline and
acetazolamide (500 mg every 6 hours), and ↑ GI losses by enteric
administration of aluminum hydroxide (30–45 ml every 6 hours).
 Aluminum hydroxide absorbs PO4 secreted into the bowel lumen and
increases PO4 loss even if none is ingested.
• HD and PD are effective in removing PO4 in Pt who have renal failure.