Efficacy and Safety of Intravenous Phosphate Replacement in Critically Ill Patients

Perreault, Marc M.; Ostrop, Nikola J; Tierney, Michael

doi:10.1177/106002809703100603

Cited by 57 publications

(22 citation statements)

References 18 publications

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“…A prospective comparative cohort study of 27 patients with severe hypophosphataemia showed the safety of administering 15-30 mmol phosphate over three hours via a central venous catheter in an intensive care unit. 16 However, the researchers reported the need for repeated doses in most patients. Terlevich et al reported efficacy of 50 mmol phosphate infused into a peripheral vein over 24 hours in 30 patients with no pre-existing renal dysfunction on general wards.…”

Section: Body Mass Index (Kg/m 2 ) <16mentioning

confidence: 99%

Refeeding syndrome: what it is, and how to prevent and treat it

Mehanna

Moledina

Travis

2008

BMJ

577

393

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Section: Body Mass Index (Kg/m 2 ) <16mentioning

confidence: 99%

Refeeding syndrome: what it is, and how to prevent and treat it

Mehanna

Moledina

Travis

2008

BMJ

577

393

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“…11,12 With regard to electrolyte repletion, numerous studies have focused on the control of a single electrolyte. [13][14][15][16] To date, 4 studies have evaluated repletion protocols for multiple electrolytes in various intensive care settings. [17][18][19][20] The results of these studies have suggested that use of repletion protocols is more effective than standard approaches to electrolyte repletion.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of an Electrolyte Repletion Protocol for Cardiac Surgery Intensive Care Patients

Couture

Létourneau²,

Dubuc

2013

CJHP

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“…Intravenous phosphate replacement may be required in these cases to correct the concentration of serum phosphate, thus ameliorating the risk of complications. 2 Although usually multifactorial in origin, the pathogenesis of hypophosphatemia includes the following mechanisms: inadequate phosphate intake, decreased intestinal absorption, gastrointestinal or renal phosphate loss, and redistribution of phosphate into cells. The latter mechanism might be the link between rapidly proliferating cells and severe hypophosphatemia as has been reported in patients suffering from hematological malignancies.…”

mentioning

confidence: 99%

Severe hypophosphatemia during hematopoietic reconstitution after allogeneic peripheral blood stem cell transplantation

Steiner

Wilhelm

et al. 2000

Bone Marrow Transplant

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Summary:A patient suffering from acute myeloid leukemia (FAB M5a) received a PBSC allograft from a matched, related donor. On day 13 after transplantation severe hypophosphatemia (0.21 mmol/l) was first noted which persisted irrespective of intravenous phosphate administration, and within 2 days reached concentrations below 0.13 mmol/l. After repeated phosphate substitution serum phosphate returned to 1.40 mmol/l on day 17. Phosphate in urine, and calcium in serum were recorded as unchanged throughout. Clinical signs and symptoms due to severe hypophosphatemia were not observed except for paresthesia in the lower extremities. The precipitous fall in serum phosphate coincided with hematopoietic reconstitution as reflected by a steep rise in leukocyte count from 0.08 × 10 9 /l on day 10 to 5.94 × 10 9 /l on day 15 after transplantation. Thus, isolated hypophosphatemia was likely the result of excessive cellular phosphate uptake during hematopoietic reconstitution. Electrolyte monitoring after PBSCT should include serum phosphate to identify the hypophosphatemia associated with hematopoietic recovery. Bone Marrow Transplantation (2000) 25, 1015-1016. Keywords: hypophosphatemia; hematopoietic reconstitution; allogeneic PBSCT The reference range for inorganic serum phosphate is 0.80-1.30 mmol/l. Mild to moderate hypophosphatemia arbitrarily defined as 0.30-0.80 mmol/l is a frequently encountered laboratory finding in hospitalized patients, whereas severe hypophosphatemia quoted as a serum concentration below 0.30 mmol/l must be considered a rare but potentially life-threatening condition. 1 Severe hypophosphatemia leads to a wide range of clinical manifestations including cardiovascular, respiratory, neuromuscular, and hematological effects. Intravenous phosphate replacement may be required in these cases to correct the concentration of serum phosphate, thus ameliorating the risk of complications. 2 Although usually multifactorial in origin, the pathogenesis of hypophosphatemia includes the following mechanisms: inadequate phosphate intake, decreased intestinal absorption, gastrointestinal or renal phosphate loss, and redistribution of phosphate into cells. The latter mechanism might be the link between rapidly proliferating cells and severe hypophosphatemia as has been reported in patients suffering from hematological malignancies. 3,4 Similarly, low serum phosphate concentrations have been reported in patients undergoing stem cell harvesting 5 or bone marrow/ peripheral blood stem cell transplantation. 6,7 Case reportA 38-year-old male patient was diagnosed in December 1998 with acute myeloid leukemia FAB M5a. He was treated with courses of cytarabine, idarubicin/cytarabine, and mitoxantrone/cytarabine, and conditioning for stem cell transplantation including total body irradiation, VP16 and cyclophosphamide. 2.97 × 10 6 /kg body weight CD34 + peripheral blood stem cells from an HLA-identical related donor were given. Therapy-associated complications included mucositis (WHO grade IV), local skin toxicity after radi...

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Efficacy and Safety of Intravenous Phosphate Replacement in Critically Ill Patients

Cited by 57 publications

References 18 publications

Refeeding syndrome: what it is, and how to prevent and treat it

Refeeding syndrome: what it is, and how to prevent and treat it

Evaluation of an Electrolyte Repletion Protocol for Cardiac Surgery Intensive Care Patients

Severe hypophosphatemia during hematopoietic reconstitution after allogeneic peripheral blood stem cell transplantation

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