Incidence Of Hypophosphataemia Research Articles

A retrospective audit to identify the incidence of hypophosphataemia following administration of Ferinject®

A retrospective audit to identify the incidence of hypophosphataemia following administration of Ferinject®

Incidencia de hipofosfatemia tras el ingreso en la Unidad de Cuidados Intensivos de pacientes en ventilación mecánica y su relación con los factores de riesgo del síndrome de realimentación

ObjectiveTo describe the incidence of hypophosphataemia in patients admitted to the ICU who have required mechanical ventilation. To analyse the presence of risk factors and its relationship with nutritional practice. DesignProspective observational study. SettingPolyvalent ICUs of two University Hospitals. PatientsPatients on invasive mechanical ventilation > 72 h with normal level of phosphorus at admission. InterventionsNone. Main variables of interestElectrolyte levels (phosphorus, magnesium, and potassium) were determined on admission to the ICU and at 96 h. Risk categories on admission, caloric intake, insulin doses and acid–base status during the first 4 days of admission were recorded. Incidence was calculated as the percentage of patients who developed hypophosphataemia after admission. Univariate analysis was performed for between-group comparison and multivariate analysis of potential risk factors. ResultsEighty nine patients were included. The incidence of hypophosphataemia was 32.6%. In these patients phosphorus decreased from 3.57 ± 1.0 mmol/L to 1.87 ± 0.65 mmol/L (52.3%). The mean kcal/kg/24 h provided in the first 4 days was 17.4 ± 4.1, with no difference between the group that developed hypophosphataemia and the group that did not. Significant risk factors were insulin doses administered and pH and PaCO2 values. ConclusionsThe incidence of hypophosphataemia at 96 h from admission in mechanically ventilated patients is high and unrelated to the risk category and hypocaloric nutritional practice used. Insulin doses and acid–base status are the main determinants of its occurrence.

Incidence and predictors of hypophosphataemia after ferric carboxymaltose use-A 3-year experience from a single institution in Singapore.

Ferric carboxymaltose (FCM) administration helps reduce transfusion requirements in the perioperative situation, which improves patient outcomes and reduces healthcare costs. However, there is increasing evidence of hypophosphataemia after FCM use. We aim to determine the incidence of hypophosphataemia after FCM administration and elucidate potential biochemical factors associated with the development of subsequent hypophosphataemia. A retrospective review of anonymised data of all FCM administrations in a single institution was conducted from August 2018 to August 2021. Each unique FCM dose administered was examined to assess its effect on Hb and serum phosphate levels within the subsequent 28 days from each FCM administration. Phosphate levels were repeatedly measured within the 28-day interval and the lowest phosphate level within that period was determined. Patients' serum phosphate levels within 28 days of FCM administration were compared against normal serum phosphate levels within 2 weeks before FCM administration. The odds ratios of various pre-FCM serum markers were calculated to elucidate potential biochemical predictors of post-FCM hypophosphataemia. In 3 years, a total of 1296 doses of FCM were administered to 1069 patients. The mean improvement in Hb was 2.45 g/dL (SD = 1.94) within 28 days of FCM administration, with the mean time taken to peak Hb levels being 6.3 days (SD = 8.63), which is earlier than expected, but was observed in this study and hence reported. The incidence of hypophosphataemia <0.8 mmol/L was 22.7% (n = 186), and <0.4 mmol/L was 1.6% (n = 9). This figure is lower than the numbers reported in previously published meta-analyses given that routine checks of serum phosphate levels were not conducted initially and hence could possibly be higher. The odds of developing hypophosphataemia (<0.8 mmol/L) were 27.7 (CI: 17.3-44.2, p < 0.0001) if baseline serum phosphate was less than 1 mmol/L. The odds of developing hypophosphataemia (<0.8 mmol/L) were 1.3 (CI: 1.08-1.59, p < 0.01) if the change in Hb levels observed after FCM administration were more than 4 g/dL. Hypophosphataemia after FCM administration is significant and FCM should be used by clinicians with caution.

Hypophosphataemia definitions, incidence and associated outcomes in paediatric intensive care: A retrospective cohort study in post-cardiac surgical patients

Hypophosphataemia has been linked to higher morbidity and mortality in intensive care but there is inconsistency in the definition of hypophosphataemia for infants and children. We aimed to determine the incidence of hypophosphataemia in a group of at-risk children in paediatric intensive care unit (PICU) and associations with patient characteristics and clinical outcomes using three different hypophosphataemia thresholds. Retrospective cohort study of 205 post-cardiac surgical patients <2 years of age admitted to Starship Child Health PICU, Auckland, New Zealand. Patient demographics and routine daily biochemistry for 14 days after PICU admission were collected. Rates of sepsis, mortality and length of mechanical ventilation were compared between groups with different serum phosphate concentrations. Out of 205 children, 6 (3%), 50 (24%) and 159 (78%) had hypophosphataemia at thresholds of <0.7, <1.0 and <1.4 mmol/L, respectively. There were no differences in gestational age at birth, sex, ethnicity or mortality in those with and without hypophosphataemia at any threshold. Children with a serum phosphate <1.4 mmol/L had more mean (SD) total hours of mechanical ventilation (85.2 (79.6) vs. 54.9 (36.2) h, P = 0.02) and those with mean serum phosphate <1.0 mmol/L had more mean hours of mechanical ventilation (119.4 (102.8) vs. 65.2 (54.8) h, P < 0.0001), episodes of sepsis (14% vs. 5%, P = 0.03) and longer length of stay (6.4 (4.8-20.7) vs. 4.9 (3.9-6.8) days, P = 0.02). Hypophosphataemia is common in this PICU cohort and serum phosphate <1.0 mmol/L is associated with increased morbidity and length of stay.

Hypophosphataemia following ferric derisomaltose and ferric carboxymaltose in patients with iron deficiency anaemia due to inflammatory bowel disease (PHOSPHARE-IBD): a randomised clinical trial

ObjectiveIntravenous iron—a common treatment for anaemia and iron deficiency due to inflammatory bowel disease (IBD)—can cause hypophosphataemia. This trial compared the incidence of hypophosphataemia after treatment with ferric carboxymaltose (FCM)...

Hypophosphataemia after treatment of iron deficiency with intravenous ferric carboxymaltose or iron isomaltoside-a systematic review and meta-analysis.

AimsHypophosphataemia is an increasingly recognized side‐effect of ferric carboxymaltose (FCM) and possibly iron isomaltoside/ferric derisomaltose (IIM), which are used to treat iron deficiency. The aim of this study was to determine frequency, severity, duration and risk factors of incident hypophosphataemia after treatment with FCM and IIM.MethodsA systematic literature search for articles indexed in EMBASE, PubMed and Web of Science in years 2005–2020 was carried out using the search terms ‘ferric carboxymaltose’ OR ‘iron isomaltoside’. Prospective clinical trials reporting outcomes on hypophosphataemia rate, mean nadir serum phosphate and/or change in mean serum phosphate from baseline were selected. Hypophosphataemia rate and severity were compared for studies on IIM vs. FCM after stratification for chronic kidney disease. Meta‐regression analysis was used to investigate risk factors for hypophosphataemia.ResultsAcross the 42 clinical trials included in the meta‐analysis, FCM induced a significantly higher incidence of hypophosphataemia than IIM (47%, 95% CI 36–58% vs. 4%, 95% CI 2–5%), and significantly greater mean decreases in serum phosphate (0.40 vs. 0.06 mmol/L). Hypophosphataemia persisted at the end of the study periods (maximum 3 months) in up to 45% of patients treated with FCM. Meta‐regression analysis identified low baseline serum ferritin and transferrin saturation, and normal kidney function as significant predictors of hypophosphataemia.ConclusionFCM is associated with a high risk of hypophosphataemia, which does not resolve for at least 3 months in a large proportion of affected patients. More severe iron deficiency and normal kidney function are risk factors for hypophosphataemia.

Hypophosphataemia after cardiopulmonary bypass – incidence and clinical significance, a South African perspective

Background: Hypophosphataemia is well-known in the intensive care units (ICU), for example, in refeeding syndrome. There is limited research available for hypophosphataemia in the ‘post-cardiac surgery’ population. Objectives: Defining the incidence of hypophosphataemia after cardiopulmonary bypass, in a South African population. Secondary objectives include the clinical implication of hypophosphataemia on duration of mechanical ventilation, ICU stay, and cardioactive drug support; and possible associations between demographic variables, intraoperative variables (including cardioplegic solution), and the postoperative phosphate levels. Methods: This was a single-centre, non-blinded, prospective cohort analytical study at an academic hospital, in patients presenting for open cardiac surgery. Over a one-year period, 101 patients were included. Preoperative variables included all the factors of the EuroSCORE II risk evaluation score. Intraoperative variables recorded were drug and blood product administration, cardioplegic solution and cardiopulmonary bypass-related variables. Postoperatively, serum phosphate levels were taken daily and postoperative care measures, such as duration of cardioactive drug support, mechanical ventilation, and ICU stay, were recorded. Results: The incidence of hypophosphataemia, immediately postoperative, was 12.6% (95% confidence interval [CI] 6.7–21.0%) and peaked on Day 3 at 29.0% (95% CI 20.1–39.4%). New onset hypophosphataemia at any stage during the ICU stay was 52.6% (95% CI 42.1–63.0%). No significant associations between hypophosphataemia and secondary objectives were found. Conclusion: Hypophosphataemia was common with an incidence higher than expected. This did not translate into a clinical effect, as the degree was usually mild (0.66–0.79 mmol/L).G

Hypophosphataemia in infants with CHD treated with amino acid infant formula.

Growth among infants with CHD is poor, and is multifactorial with multiple contributing factors. Unexplained hypophosphataemia has been reported among infants and children with complex medical needs consuming amino acid infant formula as the sole source of nutrition. The aim of this audit was therefore to review the incidence of hypophosphataemia among infants with CHD. The use of an electronic patient record search for "amino acid infant formula", "CHD", and "cardiac" yielded 136 infants 1 year of age (n=11) and infants with a structurally normal heart (n=31) were excluded from the study. The remaining 66 infants with CHD were given amino acid infant formula.Measurements and main resultsIn all, 1059 serum phosphate measures were available. After the introduction of amino acid infant formula, significantly more infants with CHD had episodes of hypophosphataemia: 15% (n=10/66) before treatment versus 29% (n=19/66) after treatment (p=0.049). Mean serum phosphate levels were significantly lower in infants with CHD following consumption of amino acid infant formula (2.0±0.5 versus 1.5±0.5 mmol/L following treatment (p<0.0001)). Infants with CHD and hypophosphataemia, associated with amino acid infant formula, use demonstrated significantly lower weight gain compared with those with normal phosphate levels (weight-for-age z scores -2.1±1.4 versus -0.9±1.5; p<0.0001). After the introduction of an amino acid formula, weight gain was significantly lower among those infants with low phosphate levels. There was a significantly higher prevalence of hypophosphataemia among infants with CHD after the introduction of amino acid infant formula. Lower phosphate levels were associated with lower weight-for-age z scores. Infants with CHD are susceptible to poor weight gain; it is therefore, crucial the nutritional status of infants prescribed amino acid infant formula is more closely monitored to ensure adequate growth.

SOME STUDIES ON HYPOPHOSPHATAEMIA IN BUFFALOES

A total number of 38 buffaloes aged between 4-7 years old with body weight ranged between 400-500kg and belonged to private farms in Ismailia Governorate were studied. Twenty of them showed the classical signs of hypophosphataemia while eight buffaloes were proved healthy by both clinical and laboratory investigations used as control group. In addition to the protective group that obtained a dose of drugs containing phosphate e.g. dibasic sod. Phosphate and eat bran in sufficient quantities and constitute Ten buffaloes. Haematological studies revealed marked decrease in erythrocytic count , haemoglobin concentration and packed cell volume in diseased animals. Biochemical analysis of blood sera showed a highly significant hypophosphataemia, hypocalcaemia and hypomagnesemia with significant increase in serum sodium and potassium levels in diseased buffaloes. In diseased Buffaloes, all parameters improved in affected buffaloes after 10 days of treatment with the use of two lines of treatment containing Tonophosphan or dibasic sodium phosphate. The protective group of buffaloes showed non significant changes in all studied parameters and pass the period of incidence of hypophosphataemia without any signs of the disease. So, prevention of hypophosphataemia can be done by giving a dose of drugs containing phosphate, and giving bran ad libidum in a balanced ration containing all necessary minerals and vitamims ,

Serum phosphate level in burn patients

Introduction Despite plasma phosphate imbalance being rare, it is a relatively common finding in certain subsets of burn patients. It may occur due to the burn itself or as a result of the treatment. Severe hypophosphataemia (<1.0 mg dl −1) is associated with a significant morbidity and a fourfold increase in mortality. In this study, the relation between serum phosphate level and the total body surface area (TBSA) of the burn was compared. Methods According to the percentage of TBSA of the burn, the patients ( n = 155) were divided into three groups: group A with 20–29% TBSA burns, group B with 30–39% and group C with more than 40% TBSA burns (62, 48 and 45 patients, respectively). Analysis of variance (ANOVA)-repeated measure was used to detect any statistically significant difference in the three post-burn time-points of 3rd, 6th and 9th days and the mean score of the serum phosphate level between the three groups. Results The incidence of hypophosphataemia at 9th post-burn day in the three groups was 6.1%, 32.4% and 73.5%, respectively. There were significant differences ( p < 0.05) between mean serum phosphate levels of groups A and C, B and C and A and B as well. We found significant differences between the three post-burn follow-up time stages. Discussion We have shown that hypophosphataemia, defined as mean serum phosphate levels below 3.0 mg dl −1, was very common following burn, based on 75.6% of patients with more than 40% burn at the 3rd post-burn day. As the percentage of TBSA of burn increases, the incidence of hypophosphataemia significantly increases. We suggest that phosphate level be routinely measured after a major burn, especially in patients with a complicated course, so that appropriate replacement therapy may be started in a timely manner.

Incidence, severity and timing of hypophosphataemia in Glasgow Royal Infirmary ICU

Hypophosphataemia is a common treatable problem in ICU, and is indicative of many pathophysiological processes that occur in critical illness. This audit's objective was to quantify the incidence, severity and timing of hypophosphataemia in the ICU. Namely, the incidence of hypophosphataemia on ICU admission and the incidence that develops following admission.

Evaluation of hypophosphataemia in tenofovir disoproxil fumarate (TDF)‐exposed and TDF‐unexposed HIV‐infected out‐patients receiving highly active antiretroviral therapy

Cases of hypophosphataemia (often coincident with renal dysfunction) have been reported in HIV-infected patients taking tenofovir disoproxil fumarate (TDF), but randomized placebo-controlled trials of HIV-infected persons with normal baseline renal function have found a comparable incidence of hypophosphataemia in the TDF and placebo groups. We assessed the incidence of grade 2 and higher hypophosphataemia in the HIV Outpatient Study (HOPS). We analysed a prospective cohort of patients who initiated either a TDF-containing highly active antiretroviral therapy (HAART) regimen [TDF-exposed (TDF+) group; n = 165] or a TDF-sparing HAART regimen [TDF-unexposed (TDF-) group; n = 90], and who had normal baseline phosphate and creatinine values. The TDF+ and TDF- groups had comparable median follow-up times (10.9 vs 8.8 months, respectively; P = 0.18) and number of phosphate measurements (median = 3 for both) and were similar on most clinical and demographic factors. During follow up, 12.7% of TDF+vs 6.7% of TDF-patients developed grade 2 hypophosphataemia (2.0-2.4 mg/dL), and 2.4% of TDF+ patients vs 0% of TDF-patients developed grade 3 hypophosphataemia (1.0-1.9 mg/dL); none developed grade 4 hypophosphataemia (<1.0 mg/dL). The incidence of grade 2 or higher hypophosphataemia was 16.7 per 100 person-years among TDF+ patients vs 8.0 per 100 person-years among TDF-patients (P = 0.11). The incidence of hypophosphataemia was somewhat elevated in HOPS patients who took TDF-containing HAART compared with those who took TDF-sparing HAART during the first 1 to 2 years of observation, but the difference was not statistically significant. Longer follow-up of a larger population is needed to determine if this trend towards an association achieves statistical significance and to evaluate the clinical consequences of hypophosphataemia.

Phosphate metabolism in red blood cells of critically ill neonates.

Very few data exist on phosphate metabolism in critically ill neonates. Therefore we studied the incidence of hypophosphataemia, the intracellular metabolism of phosphate by measuring adenosine 5'-triphosphate (ATP) and 2,3-diphosphoglycerate (2,3-DPG) in red blood cells, and excretion of phosphate in urine. The aims of the study were early detection of changes in phosphate metabolism as possible diagnostic markers of sepsis and defining the cause of hypophosphataemia.Neonates, treated in multidisciplinary paediatric intensive care unit (PICU), included in the study, were less than three days of age. Eighteen of them had respiratory distress syndrome (RDS) and 16 had microbiologically confirmed or clinical sepsis. The overall incidence of hypophosphataemia in critically ill neonates was over 80%, and was more common (88%) and more profound in those with sepsis than in those with RDS (79%). Therefore the septic neonates needed significantly larger amounts of phosphate to maintain normophosphataemia. In septic neonates ATP concentration in red blood cells was significantly lower than in neonates with RDS and controls, while the 2,3-DPG concentration was increased as a result of compensation. In septic neonates urinary losses of inorganic phosphate (Pi) were significantly higher than in neonates with RDS. Hypophosphataemia in critically ill neonates is at least partly due to higher urinary losses of phosphate.

Cardiovascular consequences of severe hypophosphataemia in brain-dead patients

Hypophosphataemia is known to induce reversible myocardial dysfunction, but the incidence of hypophosphataemia and its effect on myocardial function during brain death are unknown. In 90 consecutive brain-dead patients, we measured plasma concentrations of phosphate and left ventricular ejection fraction area (LVEFa), using transoesophageal echocardiography. In 15 severely hypophosphataemic (< 0.40 mmol litre-1), consecutive, brain-dead patients, haemodynamic status, LVEFa, and oxygen delivery and consumption were assessed before and after phosphorus loading (0.30 mmol kg-1). In 10 other brain-dead patients, urine elimination of phosphates was measured. Only 30 (33%) brain-dead patients had normal plasma phosphate concentrations, 22 (24%) had mild hypophosphataemia (0.40-0.80 mmol litre-1) and 38 (42%) had severe hypophosphataemia (< 0.40 mmol litre-1). There were no significant differences in LVEFa between these three groups (mean 53 (SD 16), 55 (12) and 51 (17)%, respectively) and no significant correlation between LVEFa and plasma phosphate concentration (r = 0.04). In 15 severely hypophosphataemic patients, phosphorus loading increased plasma phosphate concentration from 0.30 (0.10) to 1.06 (0.41) mmol litre-1, but did not modify haemodynamic status, LVEFa or oxygen delivery and consumption. In 10 other patients, urine phosphorus elimination was 16.8 (23.3) mmol/24 h while plasma phosphate concentration was at its highest level (0.80 (0.37) mmol litre-1), and only one of these patient had a slightly elevated phosphaturia. In conclusion, hypophosphataemia frequently occurs after brain death but has no significant cardiovascular consequences, suggesting that it is related to intracellular transfer and not phosphorus depletion.(ABSTRACT TRUNCATED AT 250 WORDS)