Hyperphosphatemia

Calcium is what bites you - Acute hyperphosphatemia chelates calcium and produces symptomatic hypocalcemia: perioral numbness and tingling, muscle cramps, carpopedal spasm, tetany, hyperreflexia, positive Chvostek and Trousseau signs, and at the severe end delirium, seizures and coma. Send an ionized calcium with the phosphate rather than relying on total calcium.

Giving calcium is a trade, not a fix - When the hypocalcemia is secondary to hyperphosphatemia, as in tumor lysis syndrome, replacing calcium drives further calcium-phosphate deposition in soft tissue and kidney and can worsen the acute kidney injury. Reserve it for symptomatic hypocalcemia or arrhythmia and monitor calcium serially afterward.

Cardiovascular baseline - Hyperphosphatemia produces hypotension and heart failure, and chronic calcium-phosphate deposition causes vascular calcification and arteriosclerosis with systolic hypertension, a widened pulse pressure and consequent left ventricular hypertrophy. Get a baseline ECG, and in the dialysis population an echo for LVH and ventricular function.

Tumor lysis syndrome is the acute presentation you will meet - Marked hyperphosphatemia with hypocalcemia, hyperkalemia and hyperuricemia. It appears about 72 hours after chemotherapy starts but can occur spontaneously. Hyperkalemia is the arrhythmia that kills, so the ECG is checked for both hyperkalemic and hypocalcemic changes. Treatment opens with rapid crystalloid volume expansion to restore GFR and clear solute.

Dialysis modality matters in tumor lysis - Intracellular ions keep being liberated, so intermittent hemodialysis allows rebound hyperkalemia and hyperphosphatemia. Continuous renal replacement therapy is the better modality for solute removal, with early hemodialysis reserved for life-threatening hyperkalemia.

Acute management when the kidneys still work - Extracellular volume expansion with saline plus a diuretic increases renal phosphate excretion. If renal function is impaired, that is an indication for hemodialysis rather than more fluid.

One preop phosphate can mislead you - Serum phosphate has a marked circadian rhythm, peaking near 3 am and bottoming near 11 am, and hemodialysis removes phosphate, so the value depends on both draw time and time since the last session. Look at serial measurements in a CKD patient rather than deciding off a single number.

Read the chemistry pattern for the cause - High BUN and creatinine with low calcium and normal-to-elevated PTH points to renal failure. High calcium alongside high phosphate points to vitamin D toxicity or milk-alkali syndrome. Low PTH with normal renal function points to hypoparathyroidism. Rhabdomyolysis shows elevated creatine phosphokinase with elevated uric acid; tumor lysis shows normal or marginally elevated creatine kinase with markedly elevated uric acid.

Post-neck-surgery hypoparathyroidism - The most common cause of hypoparathyroidism is injury to or removal of the parathyroid glands during thyroidectomy or other anterior neck surgery, and it presents with hyperphosphatemia, hypocalcemia, paresthesias, muscle cramps, seizures and laryngospasm. In a post-thyroidectomy patient with stridor, hypocalcemic laryngospasm belongs on the differential next to hematoma and recurrent laryngeal nerve injury.

Rule out the artifact - Pseudohyperphosphatemia is an assay interference seen with hyperglobulinemia, hyperlipidemia and hyperbilirubinemia. Repeat the measurement before treating a value that does not fit the clinical picture.

Drug and intake causes - Phosphate-containing laxatives and enemas, vitamin D intoxication, and as adverse reactions penicillin, corticosteroids, furosemide and thiazides. Chronic control is dietary restriction to 800 to 1000 mg/day plus phosphate binders, which are added when levels stay elevated or present above 6 mg/dL.

Normal adult plasma inorganic phosphate is 2.5 to 4.5 mg/dL; above 4.5 mg/dL is hyperphosphatemia. Children run higher, 4 to 7 mg/dL. Phosphate is predominantly an intracellular anion, with 85% of body stores locked in bone hydroxyapatite, and the kidneys clear about 90% of the daily load. Serum phosphate therefore does not rise until the GFR falls below roughly 30 mL/min, which is why renal failure is by far the most common cause — prevalence runs 50% to 74% in end-stage renal disease.

The acute version comes from massive tissue breakdown dumping intracellular phosphate into the extracellular space: rhabdomyolysis, tumor lysis syndrome, severe hemolysis. The perioperative consequence is not the phosphate itself but what it does to calcium — excess phosphate precipitates with calcium, dropping ionized calcium and depositing calcium-phosphate complexes in vessels and soft tissue.