Changes of serum phosphorus level in critically ill children with acute respiratory failure: a prospective observational cohort study
Keywords:hypophosphatemia, acute respiratory failure, children
Background. Severe hypophosphatemia lead to life-threatening complications. There is a little knowledge about impact of hypophosphatemia on long-term outcomes in children on mechanical ventilation. The aim of this study was to investigate the prevalence, causes and risk factors of hypophosphatemia in children with acute respiratory failure. Materials and methods. We complete a prospective single-center cohort study (May 2018 — May 2019) at the Department of Anesthesiology and Intensive Care, Danylo Halytsky Lviv National Medical University; Department of Anesthesiology and Intensive Care, Lviv Regional Children’s Hospital “OCHMATDYT”. We have examined patients aged 1 month to 3 years old with acute respiratory failure on invasive mechanical ventilation. Serum phosphorus level was evaluated on days 1, 3, 5, 7 and 9. Results described in this article is the part of the clinical study “Diaphragm ultrasound and trends in electrolyte disorders and transthyretin level as a method to predict ventilation outcome in children: the prospective observational cohort study”; ISRCTN84734652. We enrolled 57 patients with acute respiratory failure, in 4 patients, phosphorus level data weren’t monitored. Thus, we included 53 children in study results analysis. Results. The causes of acute respiratory failure in children were: acute heart failure — 2 cases (3.8 %); sepsis — 5 (9.4 %); septic shock — 10 (18.9 %); encephalopathy — 4 (7.5 %); pneumonia — 36 (67.9 %); acute obstructive bronchitis/bronchiolitis/bronchial asthma — 6 (11.3 %); bronchopulmonary dysplasia — 2 (3.8 %). All patients were divided into groups according to phosphorus level at admission. As a result, in 6 patients with normophosphatemia at admission, phosphorus level decreased to 0.9 mmol/l on day 3, to 0.75 mmol/l on day 5 and to 0.72 mmol/l and 0.65 mmol/l on days 7 and 9, respectively. In patients with mild hypophosphatemia at admission (n = 31; phosphorus level 0.68 ± 0.09 mmol/l), levels of phosphorus on days 3 and 5 were 0.42 ± 0.05 mmol/l and 0.40 ± 0.07 mmol/l, respectively. Moreover, on day 7 it reached level of severe hypophosphatemia (0.30 ± 0.04 mmol/l), and on day 9 slightly increased to 0.38 ± 0.08 mmol/l. In patients with severe hypophosphatemia at admission (n = 16; phosphorus level 0.22 ± 0.04 mmol/l), phosphorus level on day 3 increased to 0.28 ± 0.03 mmol/l, and remained virtually unchanged on days 5, 7 and 9. Conclusions. The incidence of hypophosphatemia in children with acute respiratory failure at admission was 88.7 %, and on day 5 of treatment increased to 100 %. The causes of hypophosphatemia were combinations of different mechanisms: phosphorus transport into the cells as a result of respiratory alkalosis, metabolic acidosis and sepsis; use of beta-adrenomimetics and steroids; refeeding syndrome as well as the inability to provide correction of hypophosphatemia with enteral nutrition alone.
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