Jaemin Lee, Minseok Jeong, Doo Sup Kim
Hypophosphatemia under this fixed high-dose FCM protocol was near-universal, often severe, and biphasic; replacement reached just over half the affected patients and usually left phosphate below threshold at the next measurement. The uncontrolled design, absent symptom data, and atypical setting preclude causal inference; these hypothesis-generating findings motivate prospective evaluation of stage-wise phosphate monitoring and of lower-risk iron formulations.
PURPOSE: Hypophosphatemia is an established effect of ferric carboxymaltose (FCM). We describe the perioperative phosphate trajectory across two staged operations under one fixed dose, and the completeness of replacement. The uncontrolled design cannot attribute the changes to FCM.
PATIENTS AND METHODS: Single-center retrospective cohort of 216 patients undergoing short-interval staged bilateral total knee arthroplasty (TKA) under a fixed 1,500 mg FCM protocol, tranexamic acid not being routinely used, with ten perioperative serum phosphate measurements. The preoperative sample preceded the first knee by a median of 37 days, and by at least eight days in 202 patients (93.5%). The primary outcome was a nadir below 2.0 mg/dL; below 1.0 mg/dL was biochemically severe.
RESULTS: A nadir below 2.0 mg/dL occurred in 196 patients (90.7%) and 62 (28.7%) reached the severe range. Phosphate fell biphasically, troughing two days after each knee. Among the 126 patients untreated before the second operation, the second-period nadir was deeper (1.60 versus 1.71 mg/dL, p < 0.001), as in the 98 threshold-matched patients. Higher FCM dose per kilogram was associated with a lower nadir, attenuating the female-sex association. Intravenous phosphate reached 111 of the 196 affected patients (56.6%); in 108 evaluable recipients it rose 0.33 mg/dL after the first dose against 0.21 mg/dL spontaneously in untreated patients, and 88 (81.5%) stayed below 2.0 mg/dL. A predischarge value existed in only 95 of 216 patients, leaving recovery unknown for over half.
CONCLUSION: Hypophosphatemia under this fixed high-dose FCM protocol was near-universal, often severe, and biphasic; replacement reached just over half the affected patients and usually left phosphate below threshold at the next measurement. The uncontrolled design, absent symptom data, and atypical setting preclude causal inference; these hypothesis-generating findings motivate prospective evaluation of stage-wise phosphate monitoring and of lower-risk iron formulations.