Acute Kidney Injury in Pediatric Patients: Diagnosis and Management in the Emergency Department (Pharmacology CME) - $75.00
Publication Date: May 2017 (Volume 14, Number 5)
CME Credits: 4 AMA PRA Category 1 Credits™, 4 ACEP Category I Credits, 4 AAFP Prescribed Credits, 4 AOA Category 2-A or 2-B Credits. CME expires 5/1/2020
Specialty CME Credits: Included as part of the 4 credits, this CME activity is eligible for 1 Pharmacology CME credit, subject to your state and institutional approval.
Daniel Mohrer, MD
Pediatric Resident, Yale-New Haven Children’s Hospital, New Haven, CT
Melissa Langhan, MD, MHS
Associate Professor of Pediatrics and Emergency Medicine; Fellowship Director, Director of Education, Pediatric Emergency Medicine, Yale University School of Medicine, New Haven, CT
Jason Greenberg, MD, MHS
Clinical Instructor, Department of Pediatrics, Yale University School of Medicine, New Haven, CT
Jeffrey Saland, MD
Chief, Pediatric Nephrology and Hypertension, Icahn School of Medicine at Mount Sinai, New York, NY
Rene G. VanDeVoorde III, MD, FAAP
Assistant Professor, Pediatrics, Vanderbilt School of Medicine, Nashville, TN
Bernarda Viteri, MD
Fellow, Pediatric Nephrology and Hypertension, Icahn School of Medicine at Mount Sinai, New York, NY
Inside This Issue
Not only can a missed diagnosis of pediatric acute kidney injury (pAKI) lead to a lifetime of chronic kidney disease (CKD) and increased mortality, but the entity is also often underdiagnosed in the ED. Unfortunately, reasons for diagnostic confusion are legion, starting with lack of sensitive and specific biomarkers for identifying kidney injury at an early stage and zero clinical agreement on a definitive classification system for AKI. While elevated serum creatinine (SCr) can give clinicians reasonably certain indications of pAKI, an increase in SCr can be delayed after injury, and without known baselines, early diagnosis can be problematic. In addition, normal SCr levels vary widely in children, and levels that appear low often provide a deceptive indication that pAKI has not occurred. Even once a definitive diagnosis of AKI is made, patients remain at risk for CKD, and consultation with a nephrologist is often indicated. This article helps clinicians make sense of the three current classification systems for pAKI and sort through its many disparate causes, as well as providing clear clinical pathways and practical solutions to pAKI's most common risk management pitfalls.
Excerpt From This Issue
An otherwise-healthy 3-year-old girl presents to the ED. According to the child’s mother, her daughter has been vomiting after meals for 3 days and has had 5 episodes of nonbloody, liquid diarrhea today. The mother also states that the girl drank only 4 oz of juice and 4 oz of water yesterday and would only drink half as much today. The girl has urinated only once today. She is afebrile, with a heart rate of 145 beats/min and a blood pressure of 80/30 mm Hg. On examination, the girl appears tired, has dry mucous membranes, and a capillary refill time of 3 seconds. She has diffuse abdominal tenderness but no costovertebral angle tenderness and no rash.
In the next room, a 16-year-old adolescent boy who was diagnosed with osteosarcoma 4 months ago and recently underwent treatment with cisplatin has presented with 1 day of diffuse abdominal and back pain associated with nausea, vomiting, and a decrease in oral intake and urine output.
Which historical or physical examination findings in these patients would warrant an evaluation for acute kidney injury? Which laboratory tests or imaging would be most useful in the diagnosis of these patients? How should the risk of kidney injury affect your medical management of these patients?
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