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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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  • B-type Natriuretic Peptide (BNP): A Potential Biomarker for Extubation Failure in Infants Following Cardiac Surgery by Jennifer Flint, Lori Erickson, Dawn Tucker, and Erica Molitor-Kirsch

    B-type Natriuretic Peptide (BNP): A Potential Biomarker for Extubation Failure in Infants Following Cardiac Surgery

    Jennifer Flint, Lori Erickson, Dawn Tucker, and Erica Molitor-Kirsch

    Background: BNP is a hormone released from the cardiac ventricles in response to increased pressure and volume overload1 and is an important biomarker in heart failure. Following congenital heart surgery, elevated BNP levels correlate with longer duration of mechanical ventilation, low cardiac output syndrome, and increased ICU length of stay2-4 Mechanical ventilation (MV) has an exaggerated impact on cardiopulmonary interactions in children with myocardial dysfunction, and extubation readiness can be difficult to determine post-operatively following congenital heart surgery.

    Hypothesis: An increase in post-extubation BNP levels can predict extubation failure and the need for reintubation within 48 hours.

    Methods:

    Design: prospective, observational, blinded pilot Participants: Infants ≤ 30 days of age with RACHS- 15 score ≥3 admitted to the PICU following congenital heart surgery

    Measurements: BNP levels were obtained on full MV just prior to weaning per standardized weaning protocol, one hour following a pressure support trial (PST), and at 2, 6, and 12 hours following extubation

    Conclusions:

    1. Patients who failed extubation had a trend towards higher BNP levels compared to those who did not fail extubation

    2. BNP levels increased in all patients with MV weaning and following extubation

    3. Single ventricle patients had higher BNP

  • Librarians Collaborate to Touch the Lives of Patients through Community Pediatricians by Keri Swaggart and Nancy Allen

    Librarians Collaborate to Touch the Lives of Patients through Community Pediatricians

    Keri Swaggart and Nancy Allen

    MCMLA 2012 Annual Meeting Presentation

  • Symptomatic Hypocalcemia During Urinary Alkalinization for Acute Aspirin Toxicity by Jennifer Flint and Bruce Banwart

    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.

  • The Life and Times of a Kansas Horse and Buggy Doctor and His Recollections on the Care of Children by Robert D. Schremmer MD and Jane F. Knapp MD

    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.

 

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