1. Discuss the typical feeding disorders seen in infant and pediatric outpatient populations. 2. Understand the integration of developmental levels and feeding skills in the infant and pediatric outpatient populations. 3. Be able to discuss the impact of medical and developmental disorders on the development of feeding skills in the infant and pediatric outpatient population. Feeding specialists should become familiar with common maternal and prenatal sequelae that occur during and after delivery when working in the neonatal intensive care unit (NICU) or on a well-baby unit. Not all these disorders or diseases affect an infant’s swallowing and feeding, although special attention should be directed toward the infant’s respiratory and cardiac systems because the coordination and endurance needed to feed successfully may be compromised as a result of poor cardiopulmonary development. There is a difference between a sick infant whose condition may decompensate because of an illness and a premature infant in stable condition. Feeding specialists should think beyond their comfort zone and provide an effective, holistic, and developmental approach to any evaluation and treatment process (see Chapters 11 and 13). Improved methods of prenatal care, ultrasound evaluations, and the ability to measure fetal lung maturity have reduced the risk associated with diabetes mellitus during pregnancy and the incidence of adverse perinatal outcomes of infants of diabetic mothers (IDMs). Strict glucose control is critical during the entire pregnancy. The most common complication of IDMs is congenital anomalies. Approximately 6% to 10% of pregnancies complicated by diabetes involve a structural abnormality directly related to glycemic control.1 The most common fetal structural defects associated with maternal diabetes malformations are cardiac malformations, neural tube defects, renal agenesis, and skeletal malformations.1 If the mother has hyperglycemia, it may result in fetal hyperglycemia and hyperinsulinemia that may lead to fetal overgrowth. These babies appear large at birth even when born prematurely. They are initially quiet and lethargic, rather than alert and robust. Poor feeding can be a major problem in IDMs. These babies feed slowly and may tire easily when beginning the feeding process. A preterm neonate is born before completing 37 weeks of gestation. Twelve percent of all U.S. births are premature, and approximately 2% occur at less than 32 weeks’ gestation. Multiple-gestation births frequently occur with prematurity in 57% of twins and 93% of triplets.2 A fetus is viable at 23 weeks. Problems that occur with prematurity may be respiratory, cardiovascular, neurologic, hematologic, nutritional, gastrointestinal, metabolic, renal, temperature regulatory, immunologic and/or ophthalmologic. A disorder of inflammation, tenderness, and pneumatosis (air in the bowel wall) of the intestine, necrotizing enterocolitis (NEC) usually is caused by an infection or decreased blood supply to the intestine. The seriousness of NEC varies. It may involve only the innermost lining or the entire thickness of the bowel. It is imperative that the physician diagnose this process as quickly as possible so that proper management is initiated. Causes of NEC are not well defined. NEC is a heterogeneous disease resulting from complex interactions ranging from mucosal injury caused by a variety of factors, including ischemia, infection, and poor host-protective mechanism(s) in response to injury.3 Infants are restricted from oral feedings and receive total parenteral nutrition. Clinical characteristics of the infant may include respiratory distress, apnea and/or bradycardia, lethargy, temperature instability, irritability, poor feeding, hypotension, and acidosis. The infant can have abdominal signs such as bloody stools, emesis, abdominal distention, and decreased or absent bowel sounds. Long-term sequelae may include strictures, short-bowel syndrome, malabsorption, chronic diarrhea, and feeding disorders. Infants with prolonged respiratory illness may have difficulty with oral feedings. They must learn to coordinate the suck-swallow-breathe sequence (see Chapter 3) and have the endurance to safely complete an entire feeding. Infants supported by mechanical ventilation for lengthy periods can develop oral aversions as well as grooving on the palate from the endotracheal tube needed to support respiration. Consistent developmental care is encouraged during intubation and ventilation. Infants with tracheotomies and ventilation may be able to eat orally after a detailed evaluation of their swallowing. Respiratory distress syndrome (RDS, also known as hyaline membrane disease) is the process of inadequate surfactant and a disease of prematurity. The incidence of RDS increases with decreasing gestational age. The pathophysiology of RDS includes surfactant deficiency, diffuse alveolar atelectasis, cell injury, and edema. Surfactant production depends on the maturity of the lung. Lack of surfactant causes a decrease in lung compliance because of collapse of the alveolar sacs. The initial signs of RDS appear shortly after birth. The infant will be tachypneic with worsening intercostal and sternal retractions, evidence of paradoxic breathing, duskiness, nasal flaring, apnea, and possible audible grunting. The key to management of these conditions is to prevent hypoxemia and acidosis, to stabilize fluid management and edema, reduce metabolic demands, and reduce lung injury. Current methods of treatment may include continuous positive airway pressure (CPAP) and positive end-expiratory pressure (PEEP) delivered mechanically. Surfactant replacement therapy, controlled delivery of oxygen, and varied methods of mechanical ventilation including high-frequency ventilation (HFV) are appropriate treatment interventions. The aim of mechanical ventilation is to reduce the risk of lung collapse, maintain alveolar inflation, and prevent or reduce lung injury. As the infant shows signs of improvement, the process of weaning from the ventilator occurs. A long-term complication from RDS is bronchopulmonary dysplasia. Infants with RDS are at risk for oral and pharyngeal abnormalities, including change in sensation from long-term devices such as orogastric tubes, nasogastric tubes, nasal cannulae, and endotracheal tubes. It is vital that they receive compassionate touch on the face and intraorally before oral feedings. A developmental approach before oral feedings will foster positive outcomes (see Chapter 13). Apnea is the cessation of airflow. It is considered pathologic if it lasts for more than 20 seconds or is accompanied by bradycardia (heart rate <100 beats/min). Premature infants frequently have periodic respirations with apneic periods of 5 to 10 seconds followed by 5 to 10 seconds of rapid breathing. These apneic periods are abnormal if they last for more than 15 seconds and are accompanied by cyanosis, pallor, hypotonia, or bradycardia. As many as 25% of all premature infants who weigh less than 1800 g (about 34 weeks’ gestational age) have at least one apneic episode. Usually, all infants at less than 28 weeks’ gestational age also have apnea.4 Apnea can be central nervous system mediated or caused by an obstruction. Mixed apnea, which is a combination of both causes, can also occur and usually starts with an obstruction that precipitates central apnea. One cause of apnea in the premature infant is immature chemocontrol of the respiratory drive. Apnea also can be caused by infections, metabolic disorder, impaired oxygenation, maternal drugs, intracranial lesions, poor temperature regulation, and GERD. Treatment of apnea includes continuous monitoring with gentle stimulation. Apnea of prematurity responds well to administration of theophylline and caffeine. These drugs stimulate the central nervous system to increase the infant’s response to carbon dioxide levels. As the infant’s respiratory control matures, the apneic periods decrease and usually disappear by weeks 34 to 35, although some infants experience apnea beyond this period. Bronchopulmonary dysplasia (BPD) may develop in premature infants with severe respiratory failure in the first weeks of life. BPD results from an abnormal development of lung tissue. Immaturity, malnutrition, oxygen toxicity, and mechanical ventilation may contribute to BPD, which is characterized by inflammation and scarring in the lungs. Broncho refers to the airways or the bronchial tubes through which the oxygen is transported to the lungs. Pulmonary refers to the alveoli where oxygen and carbon dioxide are exchanged. Dysplasia means abnormal changes in the structure or organization of a group of cells. The cell changes in BPD take place in the smaller airways and lung alveoli, making breathing difficult and causing problems with lung function. Prolonged hyperoxia begins a sequence of lung injury that can lead to inflammation, diffuse alveolar damage, and pulmonary dysfunction. Infants with severe BPD may depend on oxygen or mechanical ventilation for months and may have symptoms of airway obstruction for years. Long-term consequences consist of pulmonary dysfunction in adolescents and young adults and potentially impaired growth and cognitive function.5 The clinical presentation usually includes tachypnea and rales on auscultation. Infants with BPD have a difficult time learning to coordinate the timing of the suck-swallow-breathe sequence and often tire easily, especially when oral feedings are first introduced. With initial feeding of infants with BPD, they present with many sucks, then a swallow, and pauses for breathing. Often there is little rhythm to their feeding attempts. The human brain is extremely fragile and is constantly developing from the time of conception. If this process in interrupted, difficulties can develop, ranging from simple to significant disorders. Table 4-1 summarizes the major events in human brain development and the peak times of occurrence. TABLE 4-1 Major Events in Human Brain Development and Peak Times of Occurrence From Volpe JJ: Neurology of the newborn, ed 4, Philadelphia, 2001, WB Saunders. The following neurologic disorders are seen most frequently in the NICU. If the infant has a small brain or the occipitofrontal circumference (OFC) is more than 2 standard deviations below the mean for age and gender, he or she is considered microcephalic.6 The risk factors for microcephaly include viral infection, metabolic conditions, medication or substance abuse, genetic conditions, and malnutrition. The fetal risk factors may be a prenatal or perinatal insult such as inflammation, hypoxia, and birth trauma. Microcephaly can be a neuronal proliferation defect that occurs between the third and fourth months of gestational age. Hydrocephalus results when there is an excess of cerebrospinal fluid (CSF) in the ventricles of the brain from a decrease in reabsorption or overproduction.7 The clinical presentation is a large head with widened sutures. The infant may exhibit full and tense fontanelles, increasing OFC, setting sun eyes, vomiting, lethargy, and irritability. If an infant has hydrocephalus, a neurosurgical consult is warranted, and placement of a ventriculoperitoneal shunt for cerebral decompression may be considered. Deficits to the infant can be sensorimotor, cognitive, or both. Periventricular leukomalacia (PVL) is the result of ischemic or necrotic periventricular white matter changes. PVL may present as multicystic encephalomalacia with or without secondary hemorrhage.8 PVL can be secondary to systemic hypotension severe enough to impair cerebral blood flow, a focal infarction or ischemia, and episodes of apnea and bradycardia. The clinical presentation may demonstrate frequent tremors or startles, irritability, and hypertonicity with or without an abnormal Moro reflex. The long-term outcomes can include spastic dysplegia, visual impairments, upper arm paresthesias, impaired intellectual development, and lower limb weakness. Outcome is based on the location and extent of the injury. Advances in fetal echocardiography have resulted in the prenatal diagnosis of many congenital heart defects, allowing parents time to make decisions about treatment before birth.9 Although significant advancements have been made in the correction of cardiac disorders, there is now evidence of neurodevelopmental complications such as seizures and sensorimotor dysfunction after neonatal heart surgery.10 Limperopoulos et al.11 studied infants who underwent their first cardiac surgery before 12 months and surgery after 12 to 18 months. They found that 37% had moderate disability and another 6% showed severe disability. The disabilities were identified as motor and cognitive impairments, including 41% with neurologic abnormalities, 42% with gross and fine motor deficiencies, and 35% with behavioral problems. A cleft lip results from failure of mesenchymal masses in the medial nasal and maxillary prominences to join.12 The overall incidence of all types of clefts is approximately 1 in 700 live births. More boys than girls are affected, but more girls than boys have a cleft palate only. Infants can have a cleft of the lip alone, palate alone, or a combination of both, either unilateral or bilateral. Good outcome is noted with a variety of surgical corrections. These infants usually are fed with special bottles and nipples. They can breastfeed for short periods to continue the bonding process, although a bottle is usually necessary for appropriate hydration and nutrition (see Chapter 13). The child with a unilateral or bilateral cleft lip and palate often presents a feeding challenge. However, when the cleft lip or palate is not part of another syndrome (see below), the management of the child is relatively simple. Babies with only a cleft lip usually are able to breastfeed or bottle feed. They require no further intervention for this difficulty. Children with cleft palate, however, almost always have difficulty achieving and maintaining an adequate suckling pattern; this is due to limited velar mechanics, which are needed for suction. Babies sometimes appear to be suckling, and mothers often have been encouraged to breastfeed. These babies lose weight quickly and are at risk for dehydration. Babies with cleft palate rarely succeed at breastfeeding.13 CLINICAL CORNER 4-1 1. What are the medical and dietary restrictions that may be associated with short-gut syndrome? 2. What may be some of the developmental challenges associated with a child who was exposed to drugs during pregnancy? 3. What may be some of the developmental challenges associated with a child who was born at a gestational age of 32 weeks? 4. What may be some of the developmental challenges associated with a child who has experienced frequent hospitalizations? 5. Why is this information important in the development of the evaluation and therapy plan?
Disorders in Infants and Children
INFANT BACKGROUND
MATERNAL CONDITIONS
Diabetes and Gestational Diabetes
PREMATURITY
Necrotizing Enterocolitis
RESPIRATORY DISORDERS
Respiratory Distress Syndrome
Apnea
Bronchopulmonary Dysplasia
NEUROLOGIC DISORDERS
Major Developmental Event
Peak Time of Occurrence
Primary neutralization
3-4 weeks of gestation
Prosencephalic development
2-3 months of gestation
Neuronal proliferation
3-4 months of gestation
Neuronal migration
3-5 months of gestation
Organization
5 months of gestation to years after birth
Myelination
Birth to years after birth
Microcephaly
Hydrocephalus
Periventricular Leukomalacia
CARDIOVASCULAR DISORDERS
CONGENITAL ANOMALIES
Cleft Lip and Cleft Palate
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