Postsurfactant slump: early prediction of neonatal chronic lung disease?

Some infants of extremely low birth weight were noted to have respiratory deterioration (increased oxygen and ventilation requirements) around day 10 after initial improvement with surfactant (Survanta) replacement therapy. To characterize this deterioration ("slump"), we reviewed antenatal, neonatal, and short-term outcome variables in infants with a birth weight of 600 to 1,000 gm enrolled in our Survanta investigational new drug treatment protocol. Over a 20-month period 58 infants were enrolled. Of those, 51 (88%) survived. Survivors were grouped by number of doses given (in the first 48 hours): Group 1 (one, two, or three doses) (n = 29), Group 2 (four doses) (n = 22). Prevention and rescue treatments were included as per dosing protocol. On day 15, one (4%) in group 1 versus ten (45%) in group 2 required a fraction of inspired oxygen > or = 0.60, p < 0.001, and alveolar-arterial oxygen difference between groups < 200, p = 0.02. Differences between groups were not accounted for by antenatal steroid use, prevention versus rescue treatment, route of delivery, infant gender, patent ductus arteriosus, air leak, or documented infection. Bronchopulmonary dysplasia at 36 weeks' post-conceptional age was more common in group 2 (p < 0.05). We conclude that (1) the need for four doses of Survanta (administered as per protocol) was an early marker for this postsurfactant slump and (2) bronchopulmonary dysplasia at 36 weeks' postconceptional age was a better discriminator of chronic lung disease in this low-birth-weight group.

Prolonged dexamethasone therapy reduces the incidence of cryotherapy for retinopathy of prematurity in infants of less than 1 kilogram birth weight with bronchopulmonary dysplasia.

To determine whether prolonged dexamethasone therapy, used in the treatment of bronchopulmonary dysplasia (BPD), affects the incidence of cryotherapy for retinopathy of prematurity, the authors conducted a retrospective review of all infants admitted to a neonatal intensive care unit between October 1988 and October 1990 (n = 957) whose birth weights were less than 1 kg (n = 90). All admissions were reviewed to determine birth weight, gestational age, survival, incidence of BPD and cryotherapy, use and duration of dexamethasone therapy, length of mechanical ventilation, continuous positive airway pressure, and additional supplemental oxygen. Of all neonatal intensive care unit admissions, 9.4% weighed less than 1 kg, and 64% survived for greater than 28 days (n = 58). Of the survivors, 82% had BPD. Cryotherapy for retinopathy of prematurity was used only in those with birth weights of less than 1 kg and with BPD. All those treated with dexamethasone (n = 23) had BPD and significantly lower gestational ages (25.6 vs 26.4 weeks) (P = .05) and birth weights (759 vs 824 g) (P < .05) than those not treated (n = 25). Dexamethasone was used in 23 of 48 infants (9 for < or = 24 days, 14 for > 24 days). Eleven required cryotherapy: 5 of 25 with no dexamethasone, 5 of 9 treated for 24 days or less, and 1 of 14 treated for longer than 24 days (P < .04). In those treated with prolonged (> 24 days) dexamethasone, cryotherapy was significantly reduced compared with those treated for shorter periods. Although the probability was significant, the 95% confidence intervals were wide.(ABSTRACT TRUNCATED AT 250 WORDS)

Origin of 46,XY/46,XY,r(19) mosaicism.

We report on a case of 46,XY/46,XY,r(19) mosaicism. The patient shows minimal clinical abnormality and the terminal deletions prerequisite for the ring formation are not microscopically discernible. The origin of the mosaicism is discussed. Firstly, the mosaicism may represent chimerism with a prezygotic origin of the ring chromosome; secondly, the ring chromosome could have arisen postzygotically; and thirdly, the ring could have been of a prezygotic origin with the apparently normal cells actually containing reopened rings. The consequences of these hypothesis on genetic counselling are discussed.

Noncardiogenic pulmonary edema following injection of methotrexate into the cerebrospinal fluid.

The most common pulmonary disorder induced by methotrexate is a gradually developing interstitial pneumonitis. The associated clinical manifestations include slowly progressive dyspnea and nonproductive cough, with extensive radiographic changes. One case has been reported following intrathecal methotrexate administration; the remainder occurred after either intravenous or oral therapy. We report two cases of rapidly developing respiratory distress following the administration of methotrexate into the cerebrospinal fluid. The clinical courses, radiologic findings, and, in one patient, the pathologic nature, are consistent with noncardiogenic pulmonary edema.