Neonatal respiratory distress: sequela of bilateral nasolacrimal duct obstruction.

Neonatal respiratory distress is a commonly seen entity whose causes are legion. Nasal obstruction secondary to intranasal masses is significant because neonates are obligate nasal breathers. Congenital nasolacrimal duct obstruction (NLDO) causing respiratory distress is an extremely rare event since most cases of NLDO do not compromise the nasal airway. We report two cases of neonatal respiratory distress secondary to bilateral NLDO with cystic mucocele formation and intranasal extension; only two similar cases have been previously described. Pertinent embryology and anatomy are reviewed as is a brief discussion of congenital NLDO. MRI and a nasal endoscopic photograph are provided demonstrating the nasolacrimal and nasal pathology. Treatment strategies are outlined. Consideration of nasolacrimal duct pathology in the differential diagnosis of neonatal respiratory distress and nasal obstruction is stressed.

Bronchial responsiveness after inhalation of cotton bract extract.

This study examined nonspecific airway responsiveness to methacholine (MC) after inhalation of cotton bract extract (CBE). In a randomized double-blind, crossover trial, 13 healthy volunteers underwent an MC inhalation challenge test prior to inhalation of CBE and normal saline solution (NSS) aerosol sham as well as 2, 8, 24, and 168 h (7 days) later. The response parameter was the concentration of MC required to induce a 25% decrement in the maximal expiratory flow at 40% of the vital capacity below total lung capacity on the partial expiratory flow-volume curve (PC25MEF40%(P]. Five of 13 subjects demonstrated a ventilatory response to CBE with a 20% or larger decrement in the MEF40%(P); no subject demonstrated such change with NSS. For the group, the maximal decrement in MEF40%(P) was to 76.5 +/- 20.3% of baseline (mean +/- SD), occurring approximately 60 to 90 min after provocation, whereas the largest decrement after normal saline was to 88 +/- 10.6% of baseline, occurring immediately after inhalation. Changes in airway responsiveness to MC were transient. For example, the PC25MEF40%(P) for the group (mean +/- SD) was 51.3 +/- 41.1 mg/ml at baseline and 25.8 +/- 30.3 and 52.2 +/- 57.3 mg/ml at 2 and 8 h. After a pre-sham baseline of 50.4 +/- 43.2 mg/ml, PC25MEF40%(P) was 57.6 +/- 83.8 and 153.8 +/- 148 mg/ml at 2 and 8 h. Repeated measures ANOVA on these acute, same-day changes (i.e., 2 and 8 h after provocation) demonstrated a statistically significant effect of CBE on airway responsiveness (p = 0.048). These data demonstrate that inhalation of CBE, in addition to bronchospasm, causes a transient increase in airway responsiveness.