Background and AimsThere is no evidence that the epinephrine-3% hypertonic saline combination is more effective than 3% hypertonic saline alone for treating infants hospitalized with acute bronchiolitis. We evaluated the efficacy of nebulized epinephrine in 3% hypertonic saline.Patients and MethodsWe performed a randomized, double-blind, placebo-controlled clinical trial in 208 infants hospitalized with acute moderate bronchiolitis. Infants were randomly assigned to receive nebulized 3% hypertonic saline with either 3 mL of epinephrine or 3 mL of placebo, administered every four hours. The primary outcome measure was the length of hospital stay.ResultsA total of 185 infants were analyzed: 94 in the epinephrine plus 3% hypertonic saline group and 91 in the placebo plus 3% hypertonic saline group. Baseline demographic and clinical characteristics were similar in both groups. Length of hospital stay was significantly reduced in the epinephrine group as compared with the placebo group (3.94 ±1.88 days vs. 4.82 ±2.30 days, P = 0.011). Disease severity also decreased significantly earlier in the epinephrine group (P = 0.029 and P = 0.036 on days 3 and 5, respectively).ConclusionsIn our setting, nebulized epinephrine in 3% hypertonic saline significantly shortens hospital stay in hospitalized infants with acute moderate bronchiolitis compared to 3% hypertonic saline alone, and improves the clinical scores of severity from the third day of treatment, but not before.Trial Registration EudraCT 2009-016042-57

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Pulmonary sequestration is an unusual cause of heart failure in infants. We report a preterm newborn with signs of congestive heart failure supposed secondary to a ductus arteriosus that was finally diagnosed as a coexistent extralobar pulmonary sequestration. In this case, Doppler echocardiography was essential for diagnosis, revealing an abnormal systemic arterial supply to the sequestered lung and abnormal venous drainage.

Chest pain is the second most common reason for referral to a pediatric cardiologist, because cardiovascular-related disorders are a major concern for children and their families when seeking medical attention. On the rare occasions when pediatric chest pain is a result of severe heart disease, it is usually associated with well-known cardiovascular risk factors such as fibrillinopathies. Type 1 fibrillinopathies are heritable disorders caused by mutations in the fibrillin genes that lead to a broad spectrum of connective tissue phenotypes ranging from Marfan syndrome, at the most severe end, to patients displaying mild marfanoid features, or milder Marfan (MM). We report the case of an adolescent patient with MM and suspected acute coronary syndrome, with chest pain and electrocardiographic changes suggestive of myocardial ischemia. Despite the low risk of coronary or aortic dissection/aneurysm in MM, these possibilities should be tested. Once they are ruled out, mitral valve prolapse should be considered as the main cause of chest pain with ischemic-like changes in the inferior electrocardiogram leads. We emphasize that clinical and echocardiographic follow-up over years is warranted in the pediatric population to ensure that the aortic root does not show progressive dilatation or a tendency to dissect. Finally, genotyping is clinically indicated for early and complete diagnosis in patients with MM as well as de novo Marfan syndrome to take advantage of educational and clinical programs for young carriers of the mutation.

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