Case Study:
It’s January, the middle of “RSV season,” when a 2-week-old infant is brought to the emergency department by his mother because he was “breathing fast all night.” His birth history is unremarkable, and his mother claims that he had been doing well until yesterday breastfeeding, urinating, and stooling regularly. In triage, physical examination is remarkable for an irritable child with a respiratory rate (RR) of 60 breaths per minute, a heart rate (HR) of 170 beats per minute, right upper extremity blood pressure of 70/50 mmHg, axillary temperature of 37°C (99°F), and oxygen saturation as determined by pulse oximetry of 85%. Skin and mucous membranes appear dry. Extremities are cool with a capillary refill time of 4 seconds. Nasal flaring and moderate intercostals retractions are noted, and expiratory wheezing is heard bilaterally. No murmur is noted, and the liver edge is 3 cm below the right costal margin.
Supplemental oxygen is administered by a facemask and SpO2 increases to 90%. The initial concerns are RSV bronchiolitis or sepsis. An inhaled albuterol treatment is started, a capillary blood gas is obtained, intravenous access is promptly accomplished, and he receives two 20 mL/kg fluid boluses with no improvement. In fact, vital signs have deteriorated to RR 60, HR 180, BP 62/38, SpO2 86%, and crackles are auscultated on repeat examination of lungs. Extremities remain cool and mottled, and liver is now 5 cm below costal margin. A chest x-ray shows a normal sized heart, prominent pulmonary vascular markings, and mild bilateral hyperinflation. Arterial blood gas results are reported as follows: pH 7.26, pCO2 20 torr, and pO2 60 torr. At this point, one of the residents asks, “Could this patient have congenital heart disease?”
Conclusion to the above case study…
The patient presented in the opening vignette was ultimately diagnosed with critical aortic stenosis. Presentation to the emergency department occurred following delayed closure of the DA. The abrupt development of symptoms and presence of hepatomegaly provided early clues to the diagnosis, but the patient’s clinical deterioration following treatment with inhaled albuterol and aggressive intravenous fluid boluses increased the likelihood of CHD. The patient was subsequently endotracheally intubated, administered PGE via continuous infusion, and transferred to a tertiary care facility for surgical correction.
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