Decision-Making Error in Platelet Transfusion Caused by EDTA-Dependent Pseudothrombocytopenia: a Case Report and Literature Review.

BACKGROUND: Ethylenediaminetetraacetic acid-dependent pseudothrombocytopenia (EDTA-PTCP) is a rare phenomenon characterized by pseudo low platelet counts when using EDTA as anticoagulant and can result in false decision making of platelet transfusion. METHODS: An application for platelet transfusion from a patient who planned to undergo spinal surgery was received by the Department of Transfusion service. The preoperative laboratory test results showed thrombocytopenia (platelet counts: 27 x 109/L). The surgeon planned to transfuse platelets before the operation to avoid bleeding in operation due to thrombocytopenia. However, the lab technologist found that there was aggregation of platelets under the microscope. Samples used with sodium citrate and heparin as anticoagulants were rechecked. RESULTS: The platelet count of the patient was normal in sodium citrate and heparin anticoagulant tubes. The patient had no history and clinical symptoms of thrombocytopenia. Therefore, the doctor canceled the platelet order. We also reviewed the relevant literature of EDTA-PTCP. CONCLUSIONS: EDTA-PTCP is rare and may result of a wrong decision of platelet transfusion. Correct understanding and treatment of this situation can avoid unnecessary platelet transfusion.

Intranasal sodium citrate in quantitative and qualitative olfactory dysfunction: results from a prospective, controlled trial of prolonged use in 60 patients.

OBJECTIVES: We have previously shown that treatment with intranasal sodium citrate may be beneficial in post-infectious olfactory dysfunction. Sodium citrate reduces free intranasal calcium and is, therefore, thought to prevent calcium-mediated feedback inhibition at the level of the olfactory receptor. We aimed to determine whether treatment with a 2-week course of intranasal sodium citrate improves quantitative olfactory function in patients with post-infectious impairment. We also aimed to determine whether sodium citrate is beneficial in treating qualitative olfactory dysfunction. METHODS: We performed a prospective, controlled study. Patients applied intranasal sodium citrate solution to the right nasal cavity for 2 weeks. The left nasal cavity was untreated and, therefore, acted as an internal control. Monorhinal olfactory function was assessed using the "Sniffin' Sticks" composite 'TDI' score, before and after treatment. The presence of parosmia and phantosmia was also assessed. RESULTS: Overall, there was a significant increase in TDI after treatment (using the best of right and left sides). Treatment with sodium citrate did not significantly improve quantitative olfactory function, compared to control. The proportion of patients reporting parosmia did not change significantly after treatment. However, there was a significant reduction in the proportion of patients reporting phantosmia, at the end of the study period. CONCLUSIONS: Treatment with intranasal sodium citrate for a period of 2 weeks does not appear to improve quantitative olfactory function in patients with post-infectious impairment, compared to control. It may, however, be beneficial in treating phantosmia, which should be further addressed in future work.

Prevention of Contrast-induced Nephropathy in Patients with Chronic Kidney Disease Undergoing Elective Coronary Angioplasty or Angiography with Sodium Potassium Citrate Solution, a Double Blind Randomized Clinical Trial.

INTRODUCTION: Contrast-induced nephropathy (CIN) is a frequent complication of contrast exposure. A recent study suggested that Na/K citrate might have a preventive role. We investigated the efficacy of Na/K citrate to prevent CIN in patients with renal dysfunction undergoing coronary intervention. METHODS: The randomized, double-blind, placebo-controlled trial included 201 patients with estimated creatinine clearance < 90 mL/ min, randomized to receive oral Na/K citrate plus saline infusion (treatment group, 104 patients) or oral water plus saline infusion (placebo group, 97 patients). CIN was defined as an absolute increase of serum creatinine ≥ 0.5 mg/dL or a relative increase ≥ 25% or a relative decrease of estimated GFR ≥ 25% within 5 days. RESULTS: CIN occurred in 22 patients (12.29%); 10 (11%) in treatment group and 12 (13.6%) in placebo group (P > .05). Post-exposure Cr values were not significantly different between the two groups (1.18 ± 0.28 mg/dL in the placebo vs. 1.15 ± 0.29 mg/dL in the treatment group, P > .05). CIN-negative patients in the treatment group showed a significantly higher increase in urine pH than that of CIN-positive patients (1.642 ± 0.577 vs. 1.20 ± 0.422, P < .05). CONCLUSION: Na/K citrate solution is not effective for prophylaxis of CIN in patients with renal dysfunction. However, a probable preventive effect might exist in a subgroup of patients with at least 1.6 units increase in urine pH values following Na/K citrate administration.