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.

Hypophosphatemia related to intravenous iron therapy with ferric carboxymaltose: A case series.

OBJECTIVES: This case series would like to highlight hypophosphatemia related to ferric carboxymaltose and its adverse clinical consequences. BACKGROUND: Intravenous iron supplementation is a good alternative to oral iron replacement in iron deficiency anaemia due to its ability to correct iron deficit with minimal infusions without incurring the gastrointestinal side effects of oral iron replacement. Ferric carboxymaltose is one common formula for intravenous iron supplementation. However, an increasingly recognised adverse side-effect of intravenous ferric carboxymaltose is hypophosphatemia. There has been increasing reports and studies highlighting hypophosphatemia related to intra-venous iron therapy. Though initially thought to be transient and asymptomatic, recent studies have shown that persistent hypophosphatemia in iron therapy can result in debilitating disease including myopathy, fractures and osteomalacia. METHODS: A retrospective analysis of all patients who had ferric carboxymaltose was performed. RESULTS: We highlight 3 cases where hyposphatemia affected the clinical outcomes. CONCLUSION: With the increased use of IV iron it is important to be aware of the high potential for hypophosphatemia secondary to ferric carboxymaltose.

Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia (BRASH) Syndrome: A Rising Entity of Severe Bradycardia.

Bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia (BRASH) syndrome is an entity recently coined to describe this clinical pentad. Although the condition is rare, early recognition is paramount. It ensures prompt appropriate intervention is administered, as conventional management for bradycardia as guided by advanced cardiac life support (ACLS) is ineffective in the BRASH syndrome. Here, we describe a case of an elderly lady with hypertension and chronic kidney disease presenting to the emergency department with dyspnoea and confusion. She was found to have bradycardia, hyperkalemia, and acute kidney injury. Notably, she had recent changes in her medications in view of poorly controlled hypertension two days before the presentation. Her Bisoprolol 5mg every morning was changed to Carvedilol 12.5mg twice daily, and Amlodipine 10mg every morning was changed to Nifedipine long-acting 60mg twice daily. Initial treatment with atropine for bradycardia was ineffective. However, when the BRASH syndrome was identified and treated, the patient's condition improved, and she averted complications such as multiorgan failure without the need for dialysis or cardiac pacing. Early detection of bradycardia via smart devices could be considered in patients at higher risk of BRASH syndrome.

Persistent acidosis and chronic kidney disease in a patient with type 1 glycogen storage disease.

Type 1 glycogen storage disease (GSDI) is a rare autosomal recessive disorder caused by glucose-6-phosphatase (G6Pase) deficiency. We discuss a case of a 29-year-old gentleman who had GSDI with metabolic complications of hypoglycemia, hypertriglyceridemia, hyperuricemia, and short stature. He also suffered from advanced chronic kidney disease, nephrotic range proteinuria, and hepatic adenomas. He presented with acute pneumonia and refractory metabolic acidosis despite treatment with isotonic bicarbonate infusion, reversal of hypoglycemia, and lactic acidosis. He eventually required kidney replacement therapy. The case report highlights the multiple contributing mechanisms and challenges to managing refractory metabolic acidosis in a patient with GSDI. Important considerations for dialysis initiation, decision for long-term dialysis modality and kidney transplantation for patients with GSDI are also discussed in this case report.

Delayed Presentation of Hemichorea in Diabetic Striatopathy.

Diabetic striatopathy is a rare condition associated with poorly controlled diabetes that can present as hyperkinetic movements. A 70-year-old Asian female was newly diagnosed with type 2 diabetes mellitus complicated by diabetic ketoacidosis when she presented with lethargy and confusion. Computed tomography and magnetic resonance imaging of the brain performed for the patient showed incidental isolated radiological features of diabetic striatopathy, even though she did not have any hyperkinetic movements. After intensive glycemic control, the patient paradoxically developed a delayed presentation of hemichorea two weeks later. Pathological findings in diabetic striatopathy suggest the contributing role of vascular microangiopathy, similar to the changes seen in proliferative diabetic retinopathy. In order to avoid precipitating hyperkinetic movements, a less intensive diabetic control could be considered for asymptomatic patients with isolated radiological features of diabetic striatopathy. This is especially important in patients at higher risk of the condition.