| Chapter 11: | The Infant |   |
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Diaphragmatic Hernia
Diaphragmatic hernia, which occurs in about 1 in 2,200 births, is an extreme emergency and must be treated and corrected immediately upon diagnosis. Herniation of abdominal contents into the thorax is caused by an incomplete embryologic formation of the diaphragm. Ninety percent of the time it occurs on the left side, slightly lateral and posterior, through the foramen of Bochdalek.
When the herniation occurs on the left side, the stomach and intestines may enter the thorax and compress the lung, pushing the mediastinum to the right. The degree of distress noted in the neonate depends on the severity of the herniation. As the neonate begins breathing, the presence of the abdominal contents compresses the lungs, making it very difficult to complete inspiration. As air further distends the intestines and stomach, compressing the lungs even more, the neonate's respiratory distress worsens.
Symptoms of diaphragmatic hernia include cyanosis, respiratory distress, a flattened abdomen, excess amniotic fluid, and bowel sounds in the chest. Chest x-rays showing the loops of bowel in the thorax serve to confirm the diagnosis. In left-sided hernias, heart sounds can be heard in the right chest; x-rays in right-sided hernias show a large density created by the liver in the right thorax.
The treatment includes immediate insertion of a nasalgastric tube attached to suction inserted to evacuate abdominal gas. Ventilation, if needed, should be done through an endotracheal tube using rates near or above 100/min, and low PIP and PEEP pressures in order to avoid barotrauma. Surgical repair of the defect should be done through the abdomen or chest, and an umbilical artery catheter should be used to monitor blood gases and pressure.
Postoperative care should last for at least 24 hours, and usually includes a chest tube, mechanical ventilation, and therapies necessary for maintaining ABG's and preventing atelectasis. Improvement in patient status can usually be seen by the third postoperative day, allowing for medications and ventilator setting to be slowly weaned.
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Bronchopulmonary Dysplasia (BPD)
Ironically, the increasingly sophisticated protocols and equipment for treating prematurely born infants have not had an impact on bronchopulmonary dysplasia--in fact, its incidence has actually increased in the last two decades. Despite advances in the study of BPD, its exact etiology remains unknown. However, most incidences of BPD occur subsequent to the treatment of RDS. Ironically, the treatment for RDS is considered to be the primary cause of BPD, which involves high pressures and high FIO2s.
The pathophysiology of BPD appears to linked to the following four factors:
- oxygen toxicity
- baratrauma
- presence of a PDA
- fluid overload
Prolonged exposure to high concentrations of oxygen leads to edema and thickening of the alveolar membrane,and ultimately to hemorrhage of the alveolar tissues, which eventually become necrotic. As the lung attempts to heal itself, the new cells are damaged by the same factors, and the disease is perpetuated.
The diagnosis of BPD can be made from a chronic need for oxygen therapy and ventilator support, and confirmed by chest x-rays and laboratory studies. Lab studies include arterial blood gas analysis, which shows evidence of chronic lung disease (ie., hypoxia, hypercarbia and increased bicarbonate levels). As the patient progresses through the disease, the ECG will show a right axis deviation of the heart and possible hypertrophy of the right ventricle.
Pulmonary function studies will show an increased respiratory rate, decreased tidal volumes, and normal minute ventilation. Airway resistance, especially the lower airways, is increased and the lung compliance is typically decreased as a result of airway and lung parenchymal damage.
Chest x-rays on neonates with a history of high FI02 and positive pressure for several days may show density in all areas with a streaking appearance to the density. The chest x-ray (CXR) characteristics in BPD are generally seen as falling into four stages:
- Stage I: In the first 3 days of life, the CXR is typical of RDS, with bilateral frosted or ground glass appearance.
- Stage II: In days 4-10 of life, the lungs become opaque with granular infiltrates that obscure the cardiac markings.
- Stage III: This occurs during the first 10-20 days of life, and begins showing multiple small cyst formations within the lung fields with a visible cardiac silhouette. There may also be some areas of lung hyperexpansion.
- Stage IV: This occurs following day 28 of life with CXRs showing an increased lung density and the formation of larger, irregular cysts.
Treatment of BPD
There are a variety of approaches to treating BPD, but the most important goal in treatment is to avoid or reduce those factors leading to its development and perpetuation. During mechanical ventilation of the neonate, the goal is to use the lowest possible airway pressures to achieve sufficient gas exchange. If possible, it is recommended to use pressures, rates, and FIO2s that maintain the PaO2 at 45 to 55 mm Hg. Transcutaneous monitors and pulse oximeters are used to maintain these parameters, and to avoid the need for numerous arterial blood gases. Besides preventive measures, treatment includes:
Mechanical ventilation: Use a endotracheal tube small enough to allow a small leak to prevent subglottic stenosis in long-term; if treatment is planned for more than 1-2 months, a tracheostomy may be preferable. Adequate humidification of inspired gases is important for avoiding mucous plugging from thickened secretions. Extubate as quickly as tolerated.
Respiratory therapy procedures: Patients generally need chest physical therapy, suctioning, and aerosolized bronchodilators.
Fluid therapy: should be aimed at maintaining adequate hydration and urination. Diuretics such as furosemide are often needed; if patients lose excess water rapidly, they may be subjected to pneumothoraces if pressures and rates are not weaned. Long-term use of diuretics calls for maintaining calcium and phosphorus levels.
Right-heart failure: Symptomatic right-sided heart failure may be treated with digoxin in addition to diuretics. BPD patients need frequent blood work, which depletes volumes, so transfusions needed to maintain a hematocrit above 40%.
Nutrition: BPD patients may require 120 to 150 cal/kg/day to achieve growth and meet needs of lung repair.
Vitamin E: deficiency tends to increase incidence of oxygen toxicity; administration of vitamin E supplements decreases lung injury caused by administration of oxygen.