BACKGROUND: Since the introduction of surgical debulking in combination with intraoperative hyperthermic intraperitoneal chemoperfusion (HIPEC) with oxaliplatin in our institution, severe hyponatremia (sodium: 126.5 +/- 3.8 mmol/L), hyperglycemia (glucose: 22.37 +/- 4.89 mmol/L), and hyperlactatemia (lactate: 3.17 +/- 1.09 mmol/L) have been observed post HIPEC. This metabolic disorder was not observed in patients in whom cisplatin or mitomycin C was used as a chemotherapeutic drug. METHODS: In order to understand the pathophysiology of this finding, an analysis of our data was made. In a first analysis, plasma sodium was corrected for hyperglycemia based on the formula of Hillier. In a second analysis, the influence of total exchangeable sodium, total exchangeable potassium, and total body water on plasma sodium concentration was modeled. RESULTS: Analysis of our data revealed a double mechanism for the observed metabolic disorder: hyperglycemia caused by dextrose 5%, which is used as a carrier for the oxaliplatin, and major loss of sodium into the dialysate (256.7 +/- 68.7 mmol). CONCLUSION: Better control of hyperglycemia and intravenous compensation of sodium loss into the dialysate can attenuate the reported biochemical disturbance.
BACKGROUND: Since the introduction of surgical debulking in combination with intraoperative hyperthermic intraperitoneal chemoperfusion (HIPEC) with oxaliplatin in our institution, severe hyponatremia (sodium: 126.5 +/- 3.8 mmol/L), hyperglycemia (glucose: 22.37 +/- 4.89 mmol/L), and hyperlactatemia (lactate: 3.17 +/- 1.09 mmol/L) have been observed post HIPEC. This metabolic disorder was not observed in patients in whom cisplatin or mitomycin C was used as a chemotherapeutic drug. METHODS: In order to understand the pathophysiology of this finding, an analysis of our data was made. In a first analysis, plasma sodium was corrected for hyperglycemia based on the formula of Hillier. In a second analysis, the influence of total exchangeable sodium, total exchangeable potassium, and total body water on plasma sodium concentration was modeled. RESULTS: Analysis of our data revealed a double mechanism for the observed metabolic disorder: hyperglycemia caused by dextrose 5%, which is used as a carrier for the oxaliplatin, and major loss of sodium into the dialysate (256.7 +/- 68.7 mmol). CONCLUSION: Better control of hyperglycemia and intravenous compensation of sodium loss into the dialysate can attenuate the reported biochemical disturbance.
Authors: Loek A W de Jong; Fortuné M K Elekonawo; Philip R de Reuver; Andre J A Bremers; Johannes H W de Wilt; Frank G A Jansman; Rob Ter Heine; Nielka P van Erp Journal: Br J Clin Pharmacol Date: 2018-10-25 Impact factor: 4.335