Apnea is the absence of respirations for a period of 20 s or if it is associated with a decrease in heart rate of 80 beats per minute and/or accompanied by cyanosis or pallor. Apnea is categorized as central apnea when it is of CNS origin. There are no respiratory efforts and no gas flow in central apnea. In obstructive apnea, there is impaired gas flow in the presence of respiratory effort. In mixed apnea, there are components of both of the above. Periodic breathing is apnea of a few seconds' duration in a 20-s span of otherwise normal breathing. In term infants, apnea is never physiologic and is usually secondary to a serious disorder.
PATHOPHYSIOLOGY Apnea and periodic breathing are thought to arise from an immature respiratory center. There is an abnormal biphasic response to hypoxia with a period of tachypnea of several seconds followed by apnea. In premature babies, there is a shift in the carbon dioxide curve so that higher levels of CO 2 are required for respiration. Airway muscle weakness, as well as skeletal muscle weakness, probably contribute to the problem. Finally, the preterm infant may have problems during the sleep-waking states in much the same way as shifts from one sleep state to another are accompanied by respiratory instability in adults.
CLINICAL FEATURES Apnea may occur during any time in the neonatal period. It is always abnormal in the first day of life. After the age of 3 days in a preterm neonate, if it is not associated with any pathologic condition, it may be called benign apnea of prematurity. Apnea is always abnormal in a term newborn. Siblings of children who have died of sudden infant death syndrome have periods of apnea. The pathologic conditions associated with apnea are as follows:
1. Central nervous system: asphyxia, cerebral infarction, hydrocephalus, intracranial hemorrhage, meningitis, and seizures
2. Cardiovascular: congestive heart failure, and patent ductus arteriosus
3. Respiratory: chronic lung disease, hypoxia, pneumonia, and obstruction
4. Digestive system: necrotizing enterocolitis, overfeeding, and vagal response to a nasogastric tube
5. Other causes: anemia, polycythemia, sepsis, temperature instability, hyponatremia, hyperkalemia, hypocalcemia, hypermagnesemia, and high serum levels of phenobarbital, diazepam, opiates, and chloral hydrate
A complete blood count, electrolytes, calcium, glucose, blood gases, drug screen, chest x-ray, electrocardiogram, lumbar puncture, EEG, and an abdominal flat-plate film may be indicated on admission. Further workup may be necessary.
TREATMENT All infants who have benign apnea of prematurity respond to tactile stimulation. When apnea is recurrent and sustained, specific treatment is indicated. The infant who presents in the emergency department should be admitted for evaluation.
Theophylline, 5 to 6 mg/kg should be administered as an oral or intravenous loading dose, followed by 2 mg/kg q 2 h as maintenance. An alternative drug is oral or intravenous caffeine citrate, 20 to 40 mg/kg as loading dose, with 2.5 to 5 mg/kg as maintenance dose.
Continuous positive airway pressure at 2 to 4 cmH2O may be applied if the above drugs do not resolve the problem.
Mechanical ventilation with endotracheal intubation should be initiated if there is prolonged apnea or repeated episodes are not responsive to the above medications. Cyanotic Newborns
Cyanosis in neonates may be central or peripheral. Central cyanosis is defined as cyanosis of the tongue, mucous membranes, and peripheral skin and indicates the presence of 5 g or more of reduced hemoglobin. Peripheral cyanosis is defined as blue discoloration confined to the skin of the extremities; the arterial saturation is greater than 94 percent. Peripheral cyanosis is common in neonates and may persist for 2 to 3 days. It is usually due to vasomotor instability secondary to a cold environment.
Normal newborn infants have a Po2 above 50 mmHg by 5 to 10 min of age; hence, it is pathologic for central cyanosis to persist beyond 20 min after birth. Diagnostic considerations in central cyanosis include right-to-left shunts, pulmonary disorders, CNS disorders, polycythemia, or shock or sepsis.
Congenital heart disease presenting with cyanosis secondary to intracardiac right-to-left shunt includes transposition of the great vessels, tricuspid atresia, truncus arteriosus, tetralogy of Fallot and total anomalous pulmonary venous return with obstruction, pulmonary atresia, and preductal coarctation.
These lung disorders associated with cyanosis include hyaline membrane disease, pneumonia, meconium aspiration syndrome, and persistent fetal circulation due to pneumonia or asphyxia. Mechanical interference with lung function by air leaks (pneumothorax), diaphragmatic hernia, lobar emphysema, or mucous plugs also causes cyanosis.
Intracerebral hemorrhage, when severe, may be associated with shock and cyanosis. The increased viscosity and stagnation of blood in polycythemia may produce cyanosis. Shock and sepsis result in alveolar hypoventilation, causing central cyanosis.
DIAGNOSTIC APPROACH TO CENTRAL CYANOSIS Neonates with cyanosis secondary to cyanotic heart disease rarely have respiratory symptoms other than tachypnea. A murmur may be present. Neonates with lung disease producing cyanosis have respiratory distress, grunting, tachypnea, and sternal and intercostal retractions. Cyanotic infants with CNS disturbances or sepsis have apnea, bradycardia, lethargy, and seizures. Neonates with methemoglobinemia have minimal distress despite their cyanotic appearance.
The "hyperoxia test" (the Pao2 in response to breathing 100% oxygen) may be of use in distinguishing heart disease from other causes of cyanosis. Neonates with cyanotic heart disease do not demonstrate any increase in Pao2 over 20 mmHg because of the right-to-left shunting of the circulation. Most neonates with lung disease, however, demonstrate an increase in Pao2 after breathing 100% oxygen for 20 min. The neonate with persistent fetal circulation, CNS disorders, polycythemia, sepsis, and shock also demonstrates an increase in Pao2. There is no response elicited in the neonate with methemoglobinemia. When a blood specimen is exposed to air, it turns pink in all the conditions described above except in methemoglobinemia, where the blood remains chocolate colored.
The chest radiograph may demonstrate pulmonary oligemia with normal heart size in tetralogy of Fallot and pulmonary or tricuspid atresia, while pulmonary vascularity is increased in transposition of great vessels, truncus arteriosus, anomalous pulmonary venous return, and hypoplastic left heart. Neonates with lung disease have radiographs that are characteristic of the underlying disease. The electrocardiogram and echocardiogram are useful in diagnosing cyanotic heart disease. Right ventricular hypertrophy may be seen in lung disease with associated pulmonary hypertension.
TREATMENT Most of the cyanotic heart diseases are amenable to palliative or corrective surgery. Infants with severe or complete right ventricular outflow obstruction are dependent on the postnatal patency of the ductus arteriosus for maintenance of adequate pulmonary blood flow and systemic oxygenation. Short-term infusions of prostaglandin E1 0.05 to 0.1 (pg/kg)/min in these infants have allowed stabilization prior to surgery.
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