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Preparing the Malnourished Patient for Parenteral Nutrition (PN)
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
How common is hypophosphatemia in our patients? A study of 10,197 hospitalized patients found an incidence of only 0.43% on admission (Camp and Allon 1990). But in a prospective cohort of ICU patients, 34% developed hypophosphatemia 1.1 days after nutritional support was started. So the sicker patients were clearly at a much greater risk.
Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Phosphorus makes up about 0.65–1.1% of the adult body (~600 g). In the adult body 85% of phosphorus is in bone and the remaining 15% is distributed in soft tissues (3). Total phosphorus concentration in whole blood is 13 mmol/l, most of which is in the phospholipids of erythrocytes and plasma lipoproteins, with approximately 1 mmol/l present as inorganic phosphate (3). P deficiency is unusual, but symptoms of hypophosphatemia are described as bone pain, irregular breathing, fatigue, anxiety, numbness, changes in body weight and skin sensitivity (7). If Ca supply is also deficient, then the condition may become severe because of increased risks of high blood pressure and bowel cancer (7). Other consequences of P deficiency are rickets in children, osteomalacia in adults, hyperparathyroidism, anorexia, anemia, muscle weakness, De Toni-Fanconi syndrome, general debility, increased susceptibility to infection, paresthesia, ataxia, confusion, and even death (3, 7–8). Ingesting dosages of P exceeding 3–4 g/day may be harmful as it can interfere with Ca absorption (7). Hyperphosphatemia or increased phosphate level in blood is found in chronic nephritis and hypoparathyroidism. It may also lead to bone loss due to hypocalcemia (8). In addition, high phosphorus intakes could decrease calcium absorption by complexing calcium in the chyme, and may be due to high levels of food phosphate additives and cola beverages in the Western diet (3).
Adolescent Medicine
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Perry B. Dinardo, Jennifer Hyland, Ellen S. Rome
Refeeding syndrome describes the electrolyte changes, fluid imbalances, and altered homeostasis that can occur in malnourished patients when nutrition rehabilitation is initiated. The incidence of refeeding syndrome among patients with EDs who are admitted to the intensive care unit is up to 10%, with severe consequences including delirium, seizures, rhabdomyolysis, cardiac arrhythmia, acute respiratory failure, and death. The most commonly reported finding in refeeding syndrome is hypophosphatemia, which can be used in some cases as a surrogate marker for refeeding syndrome. Studies of patients with BMI < 15.1 kg/m2 have identified hypophosphatemia in up to 27% within the first week of nutrition rehabilitation. Patients with severe hypophosphatemia have a significantly increased risk of mortality. Other electrolyte disturbances commonly seen in refeeding syndrome include hypokalemia, hypomagnesemia, hyperglycemia, and thiamine deficiency.
Incidence, evolution and risk factors of hypophosphatemia in patients with solid tumors receiving ferric carboxymaltose: a retrospective cohort study
Published in Acta Clinica Belgica, 2023
Alexander Decruyenaere, Koen Kortbeek, Sigurd Delanghe, Sylvie Rottey, Hannelore Denys, Lore Lapeire
Some authors have disputed the clinical relevance of transient hypophosphatemia based exclusively on laboratory measurement of serum phosphorus [14,17]. An individual patient data meta-analysis retrospectively identified potential signs and symptoms of hypophosphatemia in 8.8% of patients receiving FCM, but did not find a correlation with the reported serum phosphorus concentration [17]. However, symptoms of hypophosphatemia that may be subtle, such as fatigue and weakness, are rarely reported as treatment-related adverse events in studies [15] and are not easily distinguishable from other causes, especially not in anemic patients undergoing anticancer therapy. Moreover, resolution of hypophosphatemia does not always reflect normalization of bone and mineral metabolism [18,19]. Ongoing or worsening fatigue, weakness or bone pain in patients receiving FCM should therefore prompt the clinician to measure serum phosphorus. A comprehensive review of clinical findings and recommendations for management are described elsewhere [15].
A rare case of parental iron-induced persistent hypophosphatemia
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Abigayle Sullivan, Theresa Lanham, Adam Rubin
Normal plasma phosphate concentration is defined as 2.5–4.5 mg/dL. Hypophosphatemia is a common finding in hospitalized patients, for which there is a wide range of causes but ultimately involves one or more of the following: decreased gastrointestinal absorption, increased renal excretion, and translocation of phosphate from intracellular to extracellular space. Various etiologies include refeeding syndrome, alcohol withdrawal, toxic shock syndrome, vitamin D-deficient rickets, McCune-Albright syndrome, X-linked hypophosphatemia, etc. [3]. Symptomatology of hypophosphatemia is dependent on the severity of the deficiency and can include severe cardiomyopathy with reduced cardiac output, hyperinsulinemia, rhabdomyolysis, hematologic abnormalities including thrombocytopenia and hemolysis, and neurologic abnormalities including ataxia, seizures, and coma [3].
Refeeding syndrome in hematological cancer patients – current approach
Published in Expert Review of Hematology, 2020
Nicola Szeja, Sebastian Grosicki
Hypophosphatemia can be caused by: low supply of phosphorus with food, absorption disorders and excessive loss of phosphorus by the kidneys. A long-term diet based on products low in phosphorus can be the cause of hypophosphatemia. Most often this applies to people with cancer, chronic alcoholism and anorexia nervosa. Other causes of phosphorus deficiency include chronic gastrointestinal diseases (which are the cause of malabsorption), vitamin D deficiency or chronic intake of medications that inhibit the absorption of phosphorus from the intestine, e.g. alkalizing drugs. Excessive phosphorus loss in urine is most often caused by hyperparathyroidism. Another cause may be kidney damage by drugs, e.g. cisplatin, aminoglycosides. The cause of phosphorus loss may also be a congenital renal tube disorder, e.g. Fanconi syndrome. The shift of phosphorus into cells is the cause of acute and often severe hypophosphatemia. It happens in people treated for diabetic ketoacidosis, in long-term starvation after restoring nutrition or after surgery to remove the parathyroid glands due to hyperthyroidism [58,68–72]. Importantly, the drugs administered during chemotherapy (bortezomib, cisplatin, imatinib, sorafenib, sunitinib) may also cause hypophosphatemia [50,68,72].