These posters have been presented at meetings in Children's Mercy and around the world. They represent research that was done at the time they were created, and may not represent medical knowledge or practice as it exists at the time viewers access these posters.
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Librarians Collaborate to Touch the Lives of Patients through Community Pediatricians
Keri Swaggart and Nancy Allen
MCMLA 2012 Annual Meeting Presentation
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Symptomatic Hypocalcemia During Urinary Alkalinization for Acute Aspirin Toxicity
Jennifer Flint and Bruce Banwart
A16y/o ingested 165 tablets of 325 mg ASA(1000 mg/kg). He presented to an outside facility 8 hours after ingestion alert with stable vital signs and ASA level 78 mg/dL. Initial lab values showed an arterial blood gas (ABG) pH 7.46, pCO2 26 mmHg, HCO3 18 mmol/L, ionized calcium 1.09 mmol/L, serum calcium 10 mg/dL, albumin 4.5 gm/dL, magnesium 2.1 mg/dL. Urinary alkalinization was initiated with a sodium bicarbonate infusion (NaHCO3) and he arrived to our facility 12 hours after ingestion with Kussmaul respirations and altered mentation. Repeat ASA 116mg/dL, ionized calcium 0.88 mmol/L and serum calcium 8.8 mg/dL. He became encephalopathic with marked hyperpnea and diaphoresis. He was not intubated due to the risk of impairing his respiratory drive and lowering his pH. Jaw thrust maneuvers were provided to maintain his airway. A dialysis catheter was placed with out sedation and dialysis was initiated. He developed bradycardia, hypotension, ST segment depression, and ventricular dysrhythmias. He required 5 liters of fluid, 3.5 gms calcium chloride, 175 mcg (3.4mcg/kg) intermittent bolus epinephrine and continuous infusions of dopamine (10 mcg/kg/min), epinephrine (0.12 mcg/kg/min), and norepinephrine (0.05 mcg/kg/min). After 3 hours of dialysis, ASA level 49 mg/dL, vital sign sstabilized, ionized calcium normalized, vasopressors were weaned off, and neurological status returned to baseline. To our knowledge, this is the first case report of urinary alkalinization leading to low ionized calcium levels with associated hemodynamic instability and dysrhythmias. Altering the serum pH during urinary alkalinization can alter the availability of ionized calcium. Urinary calcium loss may be enhanced by the excretion of the sodium load from a NaHCO3 infusion due to inhibition of calcium reabsorption in the proximal and late distal tubule, contributing to total calcium losses. The degree of insensible losses and volume depletion can be under appreciated in the setting of acute aspirintoxicity. Hypocalcemia in combination with volume depletion and rapid volume shifts seen with initiation of dialysis can lead to significant hemodynamic instability.
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The Life and Times of a Kansas Horse and Buggy Doctor and His Recollections on the Care of Children
Robert D. Schremmer MD and Jane F. Knapp MD
Describes the career of Arthur Emmanuel Hertzler, MD, 1870-1946, who practiced in Halstead, Kansas.
