Pneumothorax also is observed after vigorous resuscitation, meconium aspiration pneumonia, pulmonary hypoplasia, and diaphragmatic hernia. Spontaneous pneumothorax is seen in fewer than 1% of deliveries and may be associated with renal malformations.
BPD is a clinical diagnosis defined by oxygen dependence at36 weeks’ postconceptual age and accompanied by characteristic clinical and radiographic findings that correspond to anatomic abnormalities. Oxygen concentrations greater than 40%are toxic to the neonatal lung. Oxygen-mediated lung injuryresults from the generation of superoxides, hydrogen peroxide, and oxygen free radicals, which disrupt membrane lipids.Assisted ventilation with high peak pressures produces barotrauma, compounding the damaging effects of highly inspiredoxygen levels. In most patients, BPD develops after ventilationfor RDS that may have been complicated by PDA or pulmonary interstitial emphysema. Inflammation from prolongedassisted ventilation and repeated systemic and pulmonaryinfections may play a major role. Failure of RDS to improveafter 2 weeks, the need for prolonged mechanical ventilation,and oxygen therapy required at 36 weeks’ postconceptual ageare characteristic of patients with RDS in whom BPD develops.BPD also may develop in infants weighing less than 1000 g whorequire mechanical ventilation for poor respiratory drive in theabsence of RDS. Fifty percent of infants of 24 to 26 weeks’ gestational age require oxygen at 36 weeks’ corrected age.
The radiographic appearance of BPD is characterized initially by lung opacification and subsequently by development of cysts accompanied by areas of overdistention and atelectasis, giving the lung a spongelike appearance. The histopathology of BPD reveals interstitial edema, atelectasis, mucosal metaplasia, interstitial fibrosis, necrotizing obliterative bronchiolitis, and overdistended alveoli.
The clinical manifestations of BPD are oxygen dependence, hypercapnia with a compensatory metabolic alkalosis, pulmonary hypertension, poor growth, and development of right-sided heart failure. Increased airway resistance with reactive airway bronchoconstriction also is noted and is treated with bronchodilating agents. Severe chest retractions produce negative interstitial pressure that draws fluid into the interstitial space. Together with cor pulmonale, these chest retractions cause fluid retention, necessitating fluid restriction and the administration of diuretics.
Patients with severe BPD may need treatment withmechanical ventilation for many months. To reduce the riskof subglottic stenosis, a tracheotomy may be indicated. To reduce oxygen toxicity and barotrauma, ventilator settingsare reduced to maintain blood gases with slightly lower Pao2 (50 mm Hg) and higher Paco2 (50 to 75 mm Hg) levels thanfor infants during the acute phase of RDS. Dexamethasonetherapy may reduce inflammation, improve pulmonaryfunction, and enhance weaning of patients from assistedventilation. However, dexamethasone may increase the riskof cerebral palsy or abnormal neuromotor developmentaloutcome. Older survivors of BPD have hyperinflation, reactive airways, and developmental delay. They are at risk for severe respiratory syncytial virus pneumonia and as infantsshould receive prophylaxis against respiratory syncytialvirus.
Retinopathy of Prematurity (Retrolental Fibroplasia)
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