Contributions
Abstract: PB1984
Type: Publication Only
Background
Ceftriaxone is a frequently used empiric antibiotic in children. Acute hemolysis is a rare side effect of ceftriaxone therapy associated with a high mortality rate.
Aims
Here, we report successful management of life-threatening ceftriaxone-induced hemolytic anemia (CIHA) in a previously healthy 5-year-old girl. We also reviewed the literature of hemolytic anemia. Careful observation is required for pediatric patients receiving ceftriaxone.
Methods
A 5-year-old female was transferred to our hospital for further treatment of a sudden episode of macroscopic hematuria, hemoglobinuria, and hemolytic anemia that developed after being given fifth dose of ceftriaxone. The previous week, she had complained of a cough and fever and had been diagnosed with tonsillopharyngitis. She had been treated with ceftriaxone (100 mg/kg/day intravenously) for 2 days as an outpatient at another center. Her symptoms worsened and the fever persisted for 3 days. Her blood tests were checked on the third day. The complete blood count included hemoglobin 11.1 g/dl, hematocrit 30%, white blood cell count 18180/μl, and platelet count 519000/μl. She was hospitalized and continued on IV ceftriaxone. She had sudden-onset pallor, fatigue, and hemoglobinuria within about 30 minutes of starting the fifth dose of IV ceftriaxone. On admission to our hospital, she was unconscious and was transferred to our pediatric intensive care unit. Her vital signs were heart rate 154/min, respiratory rate 26/min, temperature 37.0°C, and blood pressure 90/60 mm Hg. The spleen was palpable 1 cm below the costal margin. She was given IV fluids and the initial laboratory tests revealed severe anemia with hemoglobin (Hb) 3.8 g/dl, hematocrit 11.1% and reticulocyte count was 3.82%. The peripheral blood smear was consistent with 4 (+) hemolysis, having schistocytes. The blood chemistry revealed indirect bilirubinemia (3.89 mg/dl; normal range: 0.3-1.1) and elevated lactate dehydrogenase (1257 U/l; normal range: 125-250). The haptoglobin level was <6.54 (normal 30–200) and Coombs’ direct antiglobulin test was positive for IgG (3+) and for C3d (3+). The reddish urine was 4 (+) for hemoglobin. CIHA was diagnosed and the ceftriaxone stopped. The patient was treated with red blood cells (10 ml/kg), high-dose immunoglobulin (1 g/kg). She improved quickly and her Hb increased from 3.8 to 7.3 g/dl. Her Hb did not drop again nor did she develop acute tubular necrosis. She was discharged on the tenth hospital day with Hb 12.7 g/dl and normal blood chemistry.
Results
The patient had no further hemolytic episodes. Her hematocrit remained stable over the following 3 months and direct antiglobulin test is still 1 (+).
Conclusion
Ceftriaxone is used very frequently in children; an early diagnosis and proper treatment of hemolytic anemia are essential to improve the patient outcome. The pathophysiological mechanism is the same as for non-drug autoimmune hemolytic anemia. However, there is still no consensus treatment for CIHA. Intravenous immunoglobulin can be used in clinical emergencies, such as our case, or in refractory cases.
Session topic: 29. Enzymopathies, membranopathies and other anemias
Keyword(s): Autoimmune hemolytic anemia (AIHA), Children, Intravenous gamma-globulin
Abstract: PB1984
Type: Publication Only
Background
Ceftriaxone is a frequently used empiric antibiotic in children. Acute hemolysis is a rare side effect of ceftriaxone therapy associated with a high mortality rate.
Aims
Here, we report successful management of life-threatening ceftriaxone-induced hemolytic anemia (CIHA) in a previously healthy 5-year-old girl. We also reviewed the literature of hemolytic anemia. Careful observation is required for pediatric patients receiving ceftriaxone.
Methods
A 5-year-old female was transferred to our hospital for further treatment of a sudden episode of macroscopic hematuria, hemoglobinuria, and hemolytic anemia that developed after being given fifth dose of ceftriaxone. The previous week, she had complained of a cough and fever and had been diagnosed with tonsillopharyngitis. She had been treated with ceftriaxone (100 mg/kg/day intravenously) for 2 days as an outpatient at another center. Her symptoms worsened and the fever persisted for 3 days. Her blood tests were checked on the third day. The complete blood count included hemoglobin 11.1 g/dl, hematocrit 30%, white blood cell count 18180/μl, and platelet count 519000/μl. She was hospitalized and continued on IV ceftriaxone. She had sudden-onset pallor, fatigue, and hemoglobinuria within about 30 minutes of starting the fifth dose of IV ceftriaxone. On admission to our hospital, she was unconscious and was transferred to our pediatric intensive care unit. Her vital signs were heart rate 154/min, respiratory rate 26/min, temperature 37.0°C, and blood pressure 90/60 mm Hg. The spleen was palpable 1 cm below the costal margin. She was given IV fluids and the initial laboratory tests revealed severe anemia with hemoglobin (Hb) 3.8 g/dl, hematocrit 11.1% and reticulocyte count was 3.82%. The peripheral blood smear was consistent with 4 (+) hemolysis, having schistocytes. The blood chemistry revealed indirect bilirubinemia (3.89 mg/dl; normal range: 0.3-1.1) and elevated lactate dehydrogenase (1257 U/l; normal range: 125-250). The haptoglobin level was <6.54 (normal 30–200) and Coombs’ direct antiglobulin test was positive for IgG (3+) and for C3d (3+). The reddish urine was 4 (+) for hemoglobin. CIHA was diagnosed and the ceftriaxone stopped. The patient was treated with red blood cells (10 ml/kg), high-dose immunoglobulin (1 g/kg). She improved quickly and her Hb increased from 3.8 to 7.3 g/dl. Her Hb did not drop again nor did she develop acute tubular necrosis. She was discharged on the tenth hospital day with Hb 12.7 g/dl and normal blood chemistry.
Results
The patient had no further hemolytic episodes. Her hematocrit remained stable over the following 3 months and direct antiglobulin test is still 1 (+).
Conclusion
Ceftriaxone is used very frequently in children; an early diagnosis and proper treatment of hemolytic anemia are essential to improve the patient outcome. The pathophysiological mechanism is the same as for non-drug autoimmune hemolytic anemia. However, there is still no consensus treatment for CIHA. Intravenous immunoglobulin can be used in clinical emergencies, such as our case, or in refractory cases.
Session topic: 29. Enzymopathies, membranopathies and other anemias
Keyword(s): Autoimmune hemolytic anemia (AIHA), Children, Intravenous gamma-globulin