SNIPPV: a new method to reduce bronchopulmonary dysplasia?

The severity of bronchopulmonary dysplasia (BPD) has decreased with recent advances in care, including surfactant treatment, but primary prevention of BPD by avoiding premature birth is still elusive. Oxygen exposure is known to be linked to the occurrence of BPD, since preterm human neonates have oxidant stress from birth. Although some neonates can develop BPD despite minimal mechanical ventilation, a significant association exists between invasive artificial ventilation and BPD. Reducing the duration of artificial ventilation by early extubation to nasal continuous positive airway pressure (NCPAP) can minimise lung injury in animal models. However, extubation failure may occur with NCPAP, mainly owing to apnoea despite caffeine treatment, which is associated with reduced BPD. Non-invasive positive pressure ventilation (NIPPV) increases successful extubation by about 30%. Although no strong evidence confirms that NIPPV reduces the occurrence of BPD, a 33% decrease in BPD may accompany the introduction of NIPPV. However, NIPPV does not ensure that the pressure is applied in synchrony with glottic opening and it may be related with gastric rupture.
A modified form of NIPPV is syncrhonised NIPPV (SNIPPV). This technique employs an abdominal pneumatic capsule to detect diaphragmatic descent, ensuring glottic patency before flow is triggered.
At present, only SNIPPV is known to be effective in weaning neonates from invasive artificial ventilation. Three controlled trials have compared SNIPPV with NCPAP after extubation in 159 preterm infants aged 1–3 weeks. The rate of weaning from invasive ventilation improved by 29%-33% with SNIPPV compared with NCPAP, with an overall SNIPPV success rate of 91%. SNIPPV was also associated to a lower incidence of BPD and, in one trial, retinopathy of prematurity. In two trials SNIPPV rescue was offered to NCPAP extubation failures and this prevented reintubation in 6/7 and 9/12 patients, respectively. These findings were confirmed in another case-controlled study comparing outcomes in neonates with a mean gestational age of 26 weeks: significant reductions in the duration of supplemental oxygen and in the incidence of BPD (73% NCPAP vs 40% SNIPPV) followed the introduction of SNIPPV. Caffeine treatment, given before extubation in this trial, may have contributed to the efficacy of non-invasive ventilation, by further decreasing BPD.
However, it should be noticed that none of these trials were specifically powered to to study the impact of SNIPPV upon the incidence of BPD. Moreover, SNIPPV has been shown to have some controindications, such as congenital airway and lung anomalies, untreated surfactant deficiency, shock/hypovolaemia/sepsis, abdominal disease/distension, haemodynamically significant patent ductus arteriosus, decreased respiratory drive, nasal trauma. This technique may also be associated to some potential short- and long-term risks (air leak, gastrointestinal distension/perforation, infection, lack of training and audit, increased requirement of nursing care, cosmetic sequelae).
In conclusion, treatment with NCPAP does not always ensure that the lungs are ‘‘opened up and kept open’’ or that hypoventilation due to apnoea is offset. The natural extension of NCPAP treatment is SNIPPV, which increases successful extubation and may reduce the incidence of BPD and perhaps that of retinopathy of prematurity. However, in neonates with respiratory distress SNIPPV should be applied with caution to those most likely to benefit from it. At present, a trial of SNIPPV powered to determine its impact on the incidence of BPD is starting. It will be important to determine how SNIPPV affects growth and development.

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