Persistent Pulmonary Hypertension

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Meconium Aspiration Syndrome

Figure 1.110. The sequelae of meconium aspiration syndrome are noted in this radiograph. There are areas of infiltrate and blebs seen in the right lung field. Pneumothorax and pneumomediastinum are common complications.

Figure 1.109. Meconium pneumonitis can occur when aspirated contents cause chemical inflammation of portions of the lung, resulting not only in hyperinflation from obstruction of airways but in patchy interstitial infiltrates extending out to the periphery. In meconium aspiration syndrome, the radiologic changes vary from lobar consolidation to widespread opacities involving both lung fields. There may be asymmetry of the patchy densities in both lung fields as seen in this radiograph. The radiologic findings in meconium aspiration syndrome may be identical to those seen in infectious pneumonia of the newborn. Aspiration pneumonitis may be secondary to esophageal atresia, pharyngeal incoordination, a vascular ring, and central nervous system abnormalities.

Figure 1.110. The sequelae of meconium aspiration syndrome are noted in this radiograph. There are areas of infiltrate and blebs seen in the right lung field. Pneumothorax and pneumomediastinum are common complications.

1.111

Persistent Pulmonary Hypertension

Figure 1.111. Persistent pulmonary hypertension of the newborn (persistent fetal circulation) is a condition in which there is persistence of the fetal high pulmonary vascular resistance. The condition can be primary, but is generally secondary to odier causes such as meconium aspiration or diaphragmatic hernia. This chest radiograph shows no significant pulmonary pathology. There is decreased vascularity with mild cardiomegaly. There is severe respiratory distress and cyanosis, and the response to oxygen is initially poor.

Figure 1.112. Medical therapy of persistent pulmonary hypertension of the newborn can cause severe complications as depicted in this radiograph. Vigorous positive pressure ventilation resulted in the development of interstitial emphysema and bilateral pneumo thoraces. Persistent shunt pathways (shunting at the foramen ovale and ductus arteriosus) and high pulmonary vascular resistance make the condition poorly responsive to medical therapy with a mortality of 30 to 50%.

Figure 1.113. Pulmonary hemorrhage frequently develops in infants with hyaline membrane disease and is common in small-for-date infants. It also occurs with other conditions such as asphyxia, cold stress, or cerebral edema. The clinical picture is that of respiratory distress associated with the coughing or aspiration of frothy bloody mucus from the trachea. Chest radiographs demonstrate homogeneous bilateral hazy infiltrates which may affect one or more pulmonary segments and give the appearance of hyaline membrane disease or consolidation. The combination of hypoxia and increased lung capillary pressure is thought to contribute to the development of this condition.

Figure 1.112. Medical therapy of persistent pulmonary hypertension of the newborn can cause severe complications as depicted in this radiograph. Vigorous positive pressure ventilation resulted in the development of interstitial emphysema and bilateral pneumo thoraces. Persistent shunt pathways (shunting at the foramen ovale and ductus arteriosus) and high pulmonary vascular resistance make the condition poorly responsive to medical therapy with a mortality of 30 to 50%.

Images Hemorraghic Diathesis

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Figure 1.114. In this gross specimen is severe hemorrhage with an irregular distribution over the surface of die lung. It may be associated with a bleeding diathesis or can occur independently. In most cases, it reflects the massive accumulation of edema thereby explaining a generally lower hematocrit in the trachea's effluent than in venous blood (about 10% lower). True hemorrhage, however, can occur.

Figure 1.114. In this gross specimen is severe hemorrhage with an irregular distribution over the surface of die lung. It may be associated with a bleeding diathesis or can occur independently. In most cases, it reflects the massive accumulation of edema thereby explaining a generally lower hematocrit in the trachea's effluent than in venous blood (about 10% lower). True hemorrhage, however, can occur.

Windsock Deformity

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