Neumayr Tara M, Gill Jeff, Fitzgerald Julie C, Gazit Avihu Z, Pineda Jose A, Berg Robert A, Dean J Michael, Moler Frank W, Doctor Allan
1Division of Critical Care Medicine, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO. 2Division of Nephrology, Hypertension, and Pheresis, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO. 3Department of Surgery, Washington University School of Medicine, St. Louis, MO. 4Department of Political Science, Washington University School of Medicine, St. Louis, MO. 5Department of Biostatistics, Washington University School of Medicine, St. Louis, MO. 6Division of Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. 7Department of Neurology, Washington University School of Medicine, St. Louis, MO. 8Department of Pediatrics, University of Utah, Salt Lake City, UT. 9Division of Critical Care Medicine, Department of Pediatrics, CS Mott Children's Hospital, University of Michigan, Ann Arbor, MI. 10Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO.
Pediatr Crit Care Med. 2017 Oct;18(10):e446-e454. doi: 10.1097/PCC.0000000000001280.
Our goal was to identify risk factors for acute kidney injury in children surviving cardiac arrest.
Retrospective analysis of a public access dataset.
Fifteen children's hospitals associated with the Pediatric Emergency Care Applied Research Network.
Two hundred ninety-six subjects between 1 day and 18 years old who experienced in-hospital or out-of-hospital cardiac arrest between July 1, 2003, and December 31, 2004.
None.
Our primary outcome was development of acute kidney injury as defined by the Acute Kidney Injury Network criteria. An ordinal probit model was developed. We found six critical explanatory variables, including total number of epinephrine doses, postcardiac arrest blood pressure, arrest location, presence of a chronic lung condition, pH, and presence of an abnormal baseline creatinine. Total number of epinephrine doses received as well as rate of epinephrine dosing impacted acute kidney injury risk and severity of acute kidney injury.
This study is the first to identify risk factors for acute kidney injury in children after cardiac arrest. Our findings regarding the impact of epinephrine dosing are of particular interest and suggest potential for epinephrine toxicity with regard to acute kidney injury. The ability to identify and potentially modify risk factors for acute kidney injury after cardiac arrest may lead to improved morbidity and mortality in this population.
我们的目标是确定心脏骤停存活儿童急性肾损伤的危险因素。
对公共访问数据集进行回顾性分析。
与儿科急诊应用研究网络相关的15家儿童医院。
296名年龄在1天至18岁之间的受试者,他们在2003年7月1日至2004年12月31日期间经历了院内或院外心脏骤停。
无。
我们的主要结局是根据急性肾损伤网络标准定义的急性肾损伤的发生情况。建立了一个有序概率模型。我们发现了六个关键解释变量,包括肾上腺素剂量总数、心脏骤停后血压、骤停位置、慢性肺部疾病的存在、pH值以及基线肌酐异常的存在。接受的肾上腺素剂量总数以及肾上腺素给药速率影响急性肾损伤风险和急性肾损伤的严重程度。
本研究首次确定了心脏骤停后儿童急性肾损伤的危险因素。我们关于肾上腺素给药影响的研究结果特别令人关注,并提示了肾上腺素对急性肾损伤的毒性可能性。识别并潜在改变心脏骤停后急性肾损伤危险因素的能力可能会改善该人群的发病率和死亡率。