Treatment of hypophosphatemia in the intensive care unit: a review

Abstract

IntroductionCurrently no evidence-based guideline exists for the approach to hypophosphatemia in critically ill patients.MethodsWe performed a narrative review of the medical literature to identify the incidence, symptoms, and treatment of hypophosphatemia in critically ill patients. Specifically, we searched for answers to the questions whether correction of hypophosphatemia is associated with improved outcome, and whether a certain treatment strategy is superior.ResultsIncidence: hypophosphatemia is frequently encountered in the intensive care unit; and critically ill patients are at increased risk for developing hypophosphatemia due to the presence of multiple causal factors. Symptoms: hypophosphatemia may lead to a multitude of symptoms, including cardiac and respiratory failure. Treatment: hypophosphatemia is generally corrected when it is symptomatic or severe. However, although multiple studies confirm the efficacy and safety of intravenous phosphate administration, it remains uncertain when and how to correct hypophosphatemia. Outcome: in some studies, hypophosphatemia was associated with higher mortality; a paucity of randomized controlled evidence exists for whether correction of hypophosphatemia improves the outcome in critically ill patients.ConclusionsAdditional studies addressing the current approach to hypophosphatemia in critically ill patients are required. Studies should focus on the association between hypophosphatemia and morbidity and/or mortality, as well as the effect of correction of this electrolyte disorder.

Refeeding hypophosphatemia: a potentially fatal danger in the intensive care unit

“…Hypophosphatemia is commonly missed due to nonspecific signs and symptoms and phosphorus level measurements are not included in most of the biochemistry panels (8 Hypophosphatemia can result in cardiac arrhythmia, respiratory failure, rhabdomyolysis, and confusion (14)(15)(16). Hypopotassemia may lead to muscle paralysis, rhabdomyolysis, muscle necrosis, respiratory failure, and myocardial contraction disorders and hypomagnesemia may cause changes in electrocardiography, tetanus, and convulsions (19).…”

Do Ionized Calcium and Phosphorus Levels have any Prognostic Value in Patients with ST-Segment Elevation Myocardial Infarction?

“…Hypophosphatemia in patients with acute myocardial infarction may be caused by a stress response that requires addition energy and involves the transfer of phosphorus into cardio-myocytes, where it is transformed into adenosine triphosphate, which binds to the damaged cellular membranes of necrotic myocytes. Increased serum catecholamine levels or metabolic acidosis can also lead to increased phosphorus loss in the urine, which can lead to or contribute to hypophosphatemia [14,19]. A positive association between increased phosphorus levels and the severity of coronary angiography findings in patients with chronic ischemic heart disease, as well as risk of death, has been found in previous studies [20,21].…”

“…Hypophosphatemia is classified as moderate (0.3 mmol/L to 0.7 mmol/L) or severe (<0.3 mmol/L). In critically ill patients, significant hypophosphatemia may contribute to rhabdomyolysis and leukocyte dysfunction as well as respiratory and heart failure [13][14][15][16]. Severe hypophosphatemia is typically observed in alcoholic patients, septic patients and patients with malnutrition or diabetic ketoacidosis, and is associated with an increased mortality risk [17,18].…”

Molecular and Biochemical Aspects of Hypophosphatemic Rickets; an Updated Review

“…In this disease, females are more affected than males. 9,10 Phosphatemia in blood, along with low level of vitamin 1,25(OH)2D and normal serum calcium levels associated with increased alkaline phosphatase activity, accompanied with normal or mild elevation of parathyroid hormone (PTH) levels can be used to differentiate XLH patients from other sorts of hypohphsphatemia. Based on the latest research, inactivating mutation of the PHEX leads to XLH and increases the FGF23 levels.…”