M. Kathleen Kelly*
INTRODUCTION
The patient group that defines Practice Pattern G are those neonates who have impaired ventilation, respiration/gas exchange, and aerobic capacity/endurance associated with respiratory failure.1 Patients are included in this practice pattern if they are younger than 4 months and present with the following risk factors or pathophysiologic processes:
•Abdominal thoracic surgeries
•Apnea and bradycardia
•Bronchopulmonary dysplasia
•Congenital anomalies
•Respiratory distress syndrome
•Meconium aspiration syndrome
•Neurovascular disorders
•Pneumonia
•Rapid desaturation with movement or crying and the following impairments, functional limitations, and disabilities:
• Abnormal pulmonary responses to activity
• Impaired airway clearance
• Impaired cough
• Impaired gas exchange
• Intercostal or subcostal retraction on inspiration
• Paradoxical or abnormal breathing pattern at rest or with activity
• Physiological intolerance of routine care
Patients older than 4 months are excluded from this pattern.
ANATOMY AND PHYSIOLOGY
Fetal to Extrauterine Transition
The transition to extrauterine life presents one of the greatest anatomic and physiologic challenges faced by an infant. At birth, a series of events must occur in order to support adequate lung and cardiac function during the conversion from liquid to air breathing and to establish parallel pulmonary and systemic circulation.2 Throughout fetal life, circulatory functions take place primarily in the placenta with relatively little blood flow through the lungs. During delivery, however, various bioch and structural changes must be initiated rapidly in order to ensure the transition from fetal to neonatal circulation. The key elements in the birth transition are the shift from maternally dependent oxygenation to continuous respiration; a switch from fetal circulation to mature circulation; the onset of independent glucose metabolism; the onset of independent oral feeding, thermoregulation, and the regulation of hormonal control of growth.3
At birth, the airways are partially filled with fluid that has been derived from the amniotic sac, tracheal glands, and lung tissue.4 The presence of this fetal lung fluid is crucial to the development of the respiratory system; however, its clearance is equally essential for the respiratory adaptations to air breathing. Within seconds of emergence from the uterine environment and the initiation of breathing, air rapidly replaces the intra-alveolar fluid. Normally, newborns rapidly establish the critical negative pressure needed to expand the alveoli and then are able to maintain adequate respiratory function and good aeration. It is only during the last few weeks of prenatal development that the lung tissue becomes fully capable of autonomous respiration—that is, gas exchange (see Table 21-1). At this time in development, the alveolar–capillary membrane thins out enough to permit gas exchange. In addition, the process of alveolarization is initiated and continues to be completed postnatally. These structural changes in the lung result in increased lung volumes and increased surface area for gas exchange. During prenatal development, a number of factors can negatively influence or affect lung development resulting in primary pulmonary hypoplasia. Secondary pulmonary hypoplasia, which is seen more often than a primary pulmonary hypoplasia, may result from an absence of fetal breathing or any restriction in the chest wall space.
TABLE 21-1 Stages of Lung Growth
In addition to the structural changes in the lung tissue that contribute to neonatal viability, surfactant production is essential to neonatal viability and morbidity. Surfactant synthesis begins at approximately 20 weeks’ gestational age and continues until the lungs are generally mature, around 35 weeks’ gestational age. Several measures of lung maturity are available, but the most widely used is the lecithin/syphingomyelin (L/S) ratio; a larger value is indicative of a more mature system. A deficiency of surfactant due to immature lungs is the hallmark of neonatal respiratory distress syndrome (RDS), a leading cause of neonatal deaths.4
During the transition from fetal to neonatal respiration, there is a large increase in pulmonary blood flow, a fall in pulmonary vascular resistance, and the establishment of lung volumes, all of which occur in the first few breaths after birth. The pressure gradient from the increased pulmonary blood flow causes the foramen ovale to close, which in turn causes right ventricular outflow to be directly diverted into the pulmonary circulation.5 Three other major structures, the ductus venosus, ductus arteriosus, and umbilical vessels, also constrict soon after birth. These closures are functional at birth, with true anatomical closure typically occurring over the next several hours and days.2
The success of the transition to extrauterine life is captured in the Apgar score (Table 21-2). This scoring system is applied to newborns in the immediate postpartum minutes and is meant to be a predictor of neonatal survival. Five easily identifiable characteristics are scored on a scale of 0, 1, or 2. These include heart rate, respiratory rate, color, reflex irritability, and tone. An Apgar score of 0 to 3 indicates the need for immediate maximal intervention including intubation and oxygen therapy; a score of 4 to 6 indicates marginal adaptation and requires stimulation, oxygen by face mask, and possibly other interventions as well as close observation; and an Apgar score of 7 to 10 indicates good adaptation to extrauterine life. At a minimum, the scores are determined at 1 minute and 5 minutes; in certain other situations an Apgar score is given at consecutive 5-minute intervals.6
TABLE 21-2 Apgar Scoring System for Newborns
Anatomic and Physiologic Features Affecting Cardiopulmonary Function in the Neonate
There are a number of age-related anatomic and physiologic differences which impact respiratory function in the neonate. These differences are most striking in premature infants and newborns and result in an increased vulnerability and susceptibility to respiratory dysfunction and cardiopulmonary compromise. Some of these differences include the following7–9:
•Small airways (increased predisposition to airway obstruction)
•Circular rib cage (decreased mechanical advantage of the diaphragm and less efficient ventilation)
•Decreased alveolar surface area
•Increased compliance of the airways (decreased bronchial stability)
•Decreased lung compliance (results in increased inflation pressures needed to maintain lung volume and resultant increased work of breathing)
•Immature neural respiratory centers (easily disrupted by drugs, sleep state, temperature)
•Susceptibility to diaphragmatic fatigue
•Irregular rate and rhythm of breathing (prone to apneic episodes)
•Compensation for respiratory insufficiency by increase in the rate, not the depth of breathing
For the otherwise healthy newborn, these developmental differences may not be problematic, but for the medically fragile or very immature infant, they can have serious consequences. There are a number of pathophysiologic processes that may result in placing a neonate in Practice Pattern 6G: Impaired Ventilation, Respiration/Gas Exchange, and Aerobic Capacity/Endurance Respiratory Failure in the Neonate. Some of the diagnoses and pathophysiologic processes that may result in respiratory failure are listed here:
•Primary lung disease
BPD (bronchopulmonary dysplasia)
Aspiration syndromes (eg, meconium aspiration)
•Persistent pulmonary hypertension
•Central nervous system disorders
Central hypoventilation syndrome (aka Ondine’s curse)
Encephalopathy, hemorrhage
•Intrinsic muscle disease
Congenital myopathies
Congenital abnormalities of the rib cage
Infantile botulism
Infantile myasthenia gravis
•Apnea of prematurity
•Congenital organ anomalies
Congenital diaphragmatic hernia
Congenital heart disease
•Congenital airway abnormalities (eg, tracheoesophageal fistula [TEF], subglottic stenosis, laryngomalacia)
Case Studies
Neonatal physical therapy is a specialty area of practice and one that requires advanced skills and competencies beyond traditional physical therapy education. Given the high-tech characteristics of the environment coupled with the unique vulnerabilities seen in an immature and fragile human, this is a challenging, but exciting environment in which to work. In both of the following cases, the infants have respiratory failure as one of their primary diagnoses; however, there are distinct differences in the pathophysiologic processes and secondary problems that they may encounter. It is noteworthy to mention that these infants may have very different courses of physical therapy interventions as they get older. This will likely depend on the degree of recovery from the acute respiratory failure and subsequent chronic lung disease and the degree of brain damage that results from the hemorrhagic or hypoxic events.
These cases illustrate the types of infants seen by physical therapists working in a neonatal intensive care unit (NICU) (see Fig. 21-1).
FIGURE 21-1 Infant in neonatal intensive care unit.
Case 1: Bronchopulmonary Dysplasia Associated with Prematurity
Sara was the 750-g product (1 lb, 10 oz) of a 26-week gestation to a 38-year-old who experienced preterm labor due to toxemia. In the delivery room, the Apgar scores were 21 55 5.10 Sara was intubated in the delivery room (DR), brought to the NICU, and stabilized. At that time umbilical artery lines were placed, a chest X-ray was taken, and surfactant was administered. After two doses of surfactant, Sara was eventually put on a ventilator because of poor oxygenation. A synchronized intermittent mandatory ventilation (SIMV) mode of mechanical ventilation was used with a rate of 25 breaths per minute; she was maintained at a SaO2 (oxygen saturation, arterial) of 93% to 95%. At day of life 1 (DOL) total parenteral nutrition was started.
Sara’s medical course was complicated by respiratory distress syndrome ultimately progressing to bronchopulmonary dysplasia. She was treated with diuretics, caffeine, inhaled aerosols, and steroids. Sara remained ventilator dependent until she was 4.5 months chronological age and was on supplemental oxygen for another 2 months. At 2.5 months of age she had a tracheostomy tube placed.
Nasogastic tube feedings were started when she was 30 weeks of gestational age (4 weeks of chronological age) and were administered until she was extubated. Nonnutritive sucking opportunities were provided while she was being fed. Once extubated, Sara began bottle-feeding, although with much difficulty secondary to decreased coordination with sucking and mainly due to poor endurance. It was noted that she desaturated during feedings and needed increased supplemental oxygen to maintain a SaO2 of 93%.
Because of her prematurity, a head ultrasound was taken on DOL 14. The scan revealed a grade IV intraventricular hemorrhage on the left and grade II intraventricular hemorrhage on the right. Sara displayed some unusual movements at approximately 2 months of age, but a neurological consult determined that she was not having seizures.
A consult from the developmental pediatrician was made to physical therapy when Sara was 2 months of chronological age. Initially, the role of the physical therapist was to assist with creating the appropriate environmental modifications. This included consulting with the nursing staff to implement a positioning program for Sara. In addition, a major component of the intervention program was teaching both the nursing staff and Sara’s parents to recognize and interpret her behavioral cues. For Sara’s parents, this helped them to better understand Sara’s physiologic status, but more importantly, they had fewer negative interactions because they could interpret her signs of “readiness” in terms of physical bonding and interactions. Once Sara was physiologically stable during position changes, gentle movement and handling was introduced in order to acclimate her to movement in general, and movement against gravity. Throughout the entire session, she was constantly monitored to ensure physiologic stability. Sara was seen several times per week by physical therapy until she was discharged at 5.5 months’ chronological age. Because of her birth history of prematurity, intraventricular hemorrhage, and bronchopulmonary dysplasia, Sara was at risk for an adverse neuromotor outcome. At the time of discharge, Sara was referred to her community-based early intervention program. The services through this program, developmental services, as well as other would be provided in her home and would include a continuation of physical therapy. The physical therapist also assisted with coordinating Sara’s discharge plans and communicating the necessary information regarding Sara’s medical issues and necessary precautions to the early intervention team. Because Sara’s parents had learned the medical aspects of her care and were able to interpret her behavioral and physiologic cues, their transition to home was relatively smooth.
Sara returned to the hospital for her follow-up visits every 3 to 6 months, and at each visit she was evaluated by the child developmental team. Over time, she had demonstrated gradual improvements in her health status. She continued to require aerosols for reactive airway disease but has had no subsequent hospitalizations. There was some concern over her growth and nutritional status because she was gaining weight slowly and by report was a slow feeder. The physical therapy examination revealed that Sara exhibited significant delays in head control, reaching and grabbing, and sitting. She had muscle tone abnormalities, presence of primitive reflexes, decreased repertoire of movement, and abnormal postural control. Sara was ultimately diagnosed with cerebral palsy.
Case 2: Full-Term Infant with Persistent Pulmonary Hypertension and Meconium Aspiration Syndrome
Joshua was a 4,200-g baby boy born at 39 weeks’ gestation via a vaginal vertex delivery to a 26-year-old. Labor lasted 24 hours, and the membranes ruptured approximately 21 hours prior to delivery. Joshua was resuscitated in the delivery room secondary to low Apgar scores of 21 25 410 and 615 after vigorous stimulation. He immediately presented with tachypnea and expiratory grunting, both of which are signs of respiratory distress. Grunting on expiration is thought to be a physiologic mechanism to prolong the expiratory phase and increase the functional residual capacity.8 Joshua was subsequently placed on 100% O2, and chest films were taken which revealed patchy infiltrates, indicative of aspiration syndrome. Pulse oximetry was 45% on room air and was unchanged on 100% O2. Arterial blood gases were drawn, and the following results were obtained:
On room air: pH 7.22/32 Paco2/41 Pao2
In 100% O2: pH 7.23/32 Paco2/44 Pao2
These results reveal a metabolic acidosis evidenced by the low pH, but more relevant was the failure to improve on 100% O2. Because of the poor oxygenation, even in the presence of 100% O2, an echocardiogram was taken to rule out congenital heart disease. The echo was negative for any cardiac abnormalities, and the diagnosis of persistent pulmonary hypertension (PPH) and meconium aspiration syndrome (MAS) was made. Joshua was sedated, intubated, and maintained on 100% O2, with ventilator settings at a rate of 40 breaths/min, and pressor support (dopamine and dobutamine) was given in order to maintain blood pressure/peripheral perfusion. Neurologic examinations over the first several days were remarkable for seizures on DOL 2; lethargy and subsequent hypotonia were noted after the first week. He was weaned from the ventilator in 7 days and was on room air by DOL 12. Joshua remained hospitalized until he was 20 days old. The pediatric neurologist consulted physical therapy on DOL 10 because of Joshua’s risk for neurologic dysfunction as a result of the hypoxia and also because of his respiratory status and ventilator dependence for a week.
EXAMINATION OF THE NEONATE WITH RESPIRATORY FAILURE
The physical therapy examination and evaluation of the neonate with respiratory failure needs to encompass a wide range of skills and observations. In addition to an understanding of cardiorespiratory anatomy and physiology in the neonate, one also needs to understand the implications of a compromise to those systems in the developing infant. In addition, knowledge of typical and atypical motor skill development is also necessary in order to interpret the examination results in light of potential functional limitations and disabilities.
The medically fragile neonate is unique with respect to anatomical, physiological, and behavioral characteristics. The immaturities in these systems and subsequent vulnerabilities related to physiologic and behavioral stability can result in the neonate easily becoming unstable during routine caregiving or social interactions. Therefore, the physical therapy examination process needs to take into account the multiple systems that interact to affect the neonate’s status. For example, it is not unusual for the fragile neonate to show signs of physiologic instability such as desaturation and increased heart rate and respiratory rate in response to a rather benign interaction such as making eye contact, being handled, or being spoken to. Thus, although our efforts may be therapeutic by design, in this particular group of patients, well-intended examination or intervention methods may result in irreparable harm.
The complexity of the technical environment also makes this a challenging population; it is essential that the physical therapist be comfortable with all of the equipment (ventilators, intravenous lines, physiologic monitoring devices). Because an infant will not communicate directly, it is up to the therapist to interpret any signs of impending or actual distress. The essence of our intervention is to ensure that no harm be done in the delivery of services and to optimize the child’s developmental potential. It is for this reason that physical therapists working with the medically fragile neonate have an advanced knowledge and understanding of the necessary competencies. Although it is outside of the scope of this chapter to cover in detail, more information on the recommended competencies for working with high-risk neonates can be found in the Practice Guidelines for the Physical Therapist in the NICU.11
Prior to beginning an examination or treatment session, the therapist should confer with the neonate’s primary nurse or caregiver to determine their most recent medical status, in addition to their baseline physiologic parameters. Depending on the nature and severity of the predisposing condition, the cardiorespiratory parameters may vary from what is considered to be normal for an infant (see Table 21-3). It is always prudent to establish the “safe” physiologic parameters within which to work. Typically, the neonate’s heart rate, respiratory rate, and oxygen saturation will be constantly monitored; however, there is no substitute for the keen visual observation of signs of distress.
TABLE 21-3 Normal Physiologic Parameters for Neonates
History
The examination process consists of three major components: history, review of systems, and specific tests and measures. Typically, the physical therapist would use the pertinent history to identify impairments, functional limitations, and disabilities in order to establish a diagnosis/prognosis and ultimately to determine the intervention. Obtaining the initial data from the medical record is a crucial first step.
Relevant data for neonates include information about maternal health, pregnancy, and delivery—specifically the birthweight, length of gestation, and the status of the baby in the immediate perinatal period. Although physical therapists are not the ones who determine the infant’s gestational age, that information is necessary for interpreting the physiologic, neurobehavioral, and musculoskeletal findings during the examination and evaluation. As well, a strong inverse correlation exists between gestational age and respiratory disease, as well as other sequelae of preterm birth. Other relevant information includes the medical and/or surgical diagnoses, current level of respiratory support, level of physiologic monitoring, medications, feeding status, and general family support issues.
Systems Review
A review of the major systems in both cases would include a general screening to determine where examination and intervention efforts should be focused. Although there were no primary pathologies or impairments of the integumentary system in either case study, it cannot be overlooked in the examination. Preterm infants in particular are prone to skin breakdown due to their extremely fragile, thin skin that contains very little subcutaneous fat. Skin inspection should be a component of the PT examination. Especially prone to damage are the areas of skin underlying the adhesive pads placed for physiologic monitoring equipment. Also, in infants with tracheostomies, the stoma is vulnerable to trauma from the moisture and friction of the tube itself and from the ties, which secure it around the neck. General vigilance regarding skin breakdown is essential if an infant is not able or capable of much active movement.
The other major systems to screen prior to organizing the PT examination would be the neuromuscular and musculoskeletal systems. In both of the cases presented, the potential exists for neuromuscular impairments secondary to the documented brain hemorrhage in the case of Sara and the neurologic involvement secondary to hypoxia in Joshua. From a musculoskeletal perspective, it would be important to rule out any obvious joint or soft tissue impairments. Although neither infant had contractures or any type of musculoskeletal defect, they were at risk for contractures secondary to their relative immobility and the gravity-dependent position in which most nursing/medical care occurs. In both cases, positioning programs were recommended and carried out by the nursing staff.
Tests and Measures
The goal of the physical therapy examination process is to identify the “impairments, functional limitations, and disabilities and establish the diagnosis and the prognosis.” The specific tests and measures are individualized with respect to the patient presentation and not to diagnosis alone. Although the diagnoses and other patient-related factors differ for the two cases presented, much is similar in terms of the tests and measures, indications for PT involvement, and expected outcomes.
One of the most important priorities and considerations when working with neonates, especially infants born prematurely like Sara, is recognition of their tolerance to handling. Thus, a critical part of the PT examination will be determining the infant’s baseline physiologic stability. At any given time, this should be preceded by a discussion with the patient’s primary nurse to determine that a true baseline is being obtained. If the baby has just had some medical intervention, for example, their physiologic status may have been affected, and the result of the PT test may reveal a “poststress” response, rather than a true baseline. This concept is not unlike that used in exercise testing, when the baseline measures are used to interpret the patient’s exercise and postexercise recovery responses. The appropriate tests and measures for Sara and Joshua are presented in Tables 21-4 through 21-7; each is followed by the examination strategy and interpretation, when necessary.
TABLE 21-4 Sara and Joshua: Tests for Assessment of Aerobic Capacity and Endurance
TABLE 21-5 Sara and Joshua: Tests for Assessment of Ventilation and Respiration/Gas Exchange
TABLE 21-6 Sara and Joshua: Tests for Behavioral Responses and Stabilitya
TABLE 21-7 Sara and Joshua: Tests for Motor Function/Neuromotor Development/Sensory Integrationa
Regardless of the reason for a neonate having respiratory failure, appreciation of the fact that the child is at a disadvantage in terms of developmental risks is a compelling reason to begin early intervention as soon as the infant or child is medically stable. Because of the risks for abnormal neurodevelopmental sequelae, physical therapists should be involved with providing developmental intervention early in the course of an infant’s hospitalization. Delays in the initiation of rehabilitation or habilitation can place the child at risk for developing preventable secondary impairments and functional limitations.
INTERVENTIONS FOR NEONATES WITH RESPIRATORY DISTRESS
In a best-practice environment, neonates with respiratory failure are managed with a multidisciplinary approach. A unique role of the physical therapist on that team is to provide interventions that are physiologically and developmentally appropriate for infants who are at risk for delayed or abnormal motor development. Physical therapists are uniquely qualified to design and implement treatment plans with outcomes directed toward movement efficiency. Thus, in the patient cases presented here, the physical therapy interventions were developmentally appropriate motor activities that were implemented and monitored in much the same way as one would monitor a cardiopulmonary rehabilitation exercise program. Tables 21-8 through 21-10 outline the various components of the physical therapy interventions for Sara and Joshua, the anticipated goals, and the specific strategies used to accomplish the goal. The anticipated goals served as a benchmark for the expected outcomes.
TABLE 21-8 Sara and Joshua Interventions: Coordination, Communication, and Documentation
TABLE 21-9 Sara and Joshua Interventions: Patient/Client-Related Instruction
TABLE 21-10 Sara and Joshua Interventions: Procedural Interventionsa
The direct interventions included goals from both the cardiopulmonary and the neuromuscular practice patterns (neuromuscular preferred Practice Pattern C:Impaired Motor Function and Sensory Integrity Associated with Nonprogressive Disorders of the Central Nervous System—Congenital Origin or Acquired in Infancy or Childhood). Activities were chosen that were developmentally appropriate while monitoring the physiologic cost to the infant. The concept of aerobic and endurance training was utilized with the strategies incorporating developmental motor skills typically acquired during the first few weeks of life.
During the initial examination, it was clear that both infants were medically fragile due to their behavioral instability and “time out” signs of stress. In both cases, the behavioral cues occurred concurrently with signs of a physiologic cost to the infant evidenced by changes in heart rate and oxygen saturation. There was constant vigilance of the physiologic monitors for both of the infants; and in fact, any changes indicative of increased stress or effort resulted in immediate modifications to the intervention.
A positioning program was instituted for both infants in which position changes were encouraged after every clustered caregiving episode. By incorporating this at a time when other caregiving occurs, the nursing staff did not feel overwhelmed with additional “duties.” The positioning program included recommendations for prone positioning, supported side-lying, supported semisitting, and supine positioning with the use of blanket rolls to provide protraction and midline orientation for the upper extremities and to decrease the tendency toward abduction and external rotation in the lower extremities (Fig. 21-2). Prone positioning, in particular, has been recently discouraged as a position for babies to sleep because of the risk of sudden infant death syndrome (SIDS); however, there are known benefits of its effects on oxygenation, heart rate, chest wall synchrony, and behavioral measures (for a review, see Refs. 8 and 19). In addition, the prone position is important for the infant to develop antigravity head control. Although there has not been evidence to support the effects of a positioning program on the musculoskeletal system, it was utilized with the assumption that it would decrease the effects of gravity on the soft tissue structures of the musculoskeletal system. For many reasons, in addition to their immature musculoskeletal systems, these infants lack strength, as evidenced by the paucity of movement against gravity.
FIGURE 21-2 Positioning strategies for neonates. (A) supine, (B) side-lying, (C) prone.
Chest physical therapy techniques were limited to the use of positioning and gentle movement transitions to mobilize secretions.
Risk Factors
Efficient respiratory function requires an organ of gas exchange, that is, the lungs, and a “pump” mechanism consisting of the rib cage and respiratory muscles, in addition to an intact neural control mechanism for respiration.20Under normal conditions, the respiratory pump can adapt to satisfy the changing metabolic needs that may occur during exercise, hyperthermia, or other demands21; but when these systems are unable to deliver oxygen and remove carbon dioxide from the pulmonary circulation, respiratory failure ensues and gas exchange is impaired.22 In the neonate, a number of anatomic and physiologic immaturities place them at risk for respiratory failure. Structurally, the infant is born with a compliant rib cage secondary to the lack of complete bony ossification. The latter, along with less compliant lung tissue and decreased muscle mass, results in inefficient respiratory mechanics. Infants also have a predisposition to diaphragmatic fatigue because of the decreased proportion of type I muscle fibers. Less than 10% of the diaphragmatic muscle fibers consist of high-oxidative and slow-twitch fibers, making them poorly equipped to handle high workloads.23
Pathophysiology of Bronchopulmonary Dysplasia
These immaturities are exacerbated only in the infant born prematurely. One of the most common and most serious sequelae of preterm birth is RDS—the most common respiratory abnormality in the preterm infant, and the single most common cause of death in neonates.4 The primary pathology in RDS is due to the decreased amount of surfactant. As a result, the infant’s pulmonary status is characterized by an increase in alveolar surface tension, alveolar collapse, diffuse atelectasis, ventilation/perfusion mismatch, and decreased lung compliance. Because of increased pulmonary artery pressures, a subsequent right-to-left shunt results in a ventilation–perfusion mismatch. Typical signs and symptoms of RDS include increased respiratory rate, retractions, nasal flaring, grunting, cyanosis, and an increased work of breathing.
The introduction of surfactant therapy has made a significant difference in the outcomes of babies like Sara with RDS.24 It is now standard practice for babies born less than 30 to 32 weeks GA to be given prophylactic surfactant administration in the delivery room within their first few breaths.25 Numerous clinical trials have established evidence for surfactant’s efficacy in improving gas exchange, reducing the severity of the acute disease and increasing survival in preterm infants.25,26 Other management strategies for babies with RDS include steroid administration, supplemental oxygenation, assisted ventilation, and nutritional intervention. As a result of these interventions, the incidence and the profile of babies like Sara who develop a form of chronic lung disease known as BPD have changed.27
Bronchopulmonary dysplasia was first described by Northway and colleagues in 1967 as a disease of preterm infants characterized by both acute lung changes and chronic lung changes with resultant inflammation of the lung parenchyma, a combination of emphysema and fibrosis, and remodeling.28 This classic form of BPD occurred primarily in preterm infants who required mechanical ventilation with high inspiratory pressures to maintain airway patency and high concentrations of supplemental oxygen, both of which were thought to contribute to its pathogenesis. The clinical diagnosis of BPD was made when the infant was oxygen dependent (greater than 30%) beyond 28 to 30 days and had accompanying radiographic changes in the lungs. The cohort of infants described in Northway’s original work was over 31 weeks of gestational age and all but one weighed more than 1,500 g.
As a result of improved, less traumatic ventilation methods, antenatal steroids, and surfactant, it is now infrequent to see BPD in babies with birth weights greater than 1,200 g and gestational ages beyond 30 weeks.29 Despite this, the incidence of BPD has not changed much because of the increased survival of smaller and more preterm babies. Similar to RDS, the risk of developing BPD increases linearly with decreasing gestational age and birth weight. Furthermore, BPD continues to be a major complication in preterm infants who require mechanical ventilation.30
More recent histopathologic findings from babies who die from respiratory complications of BPD have revealed a newer and different profile of BPD. No longer are the prominent findings related to airway and lung tissue trauma and inflammation; rather, less fibrosis and more uniform inflation are noted.31 In addition, the major manifestation of lung injury seems to be an interruption in lung development. These very recent findings have forced a major reconsideration of the pathogenesis, diagnosis, management, and long-term outcomes of infants with BPD. As well, a newer clinical definition of BPD has emerged, as the original definition would only apply to a small number of babies. A very recent workshop on BPD summarized a new definition of BPD that also provides a classification of severity based on the need for supplemental oxygen and/or positive pressure ventilation29 (Table 21-11).
TABLE 21-11 Newly Proposed Guidelines for Classification of BPDa
Treatment of Bronchopulmonary Dysplasia
The treatment of BPD includes nutritional support to promote lung development and maturation, fluid management, pharmacologic management, and respiratory support. Commonly used pharmacologic approaches include bronchodilators and diuretics to improve airway conductance, decrease edema, and increase gas exchange; sedatives for persistent agitation; and high-dose corticosteroids to decrease inflammation of the respiratory tract. The respiratory management may range from supplemental oxygen given by nasal cannula to a tracheostomy and mechanical ventilation.
Because lung tissue continues to grow postnatally, most infants recover from BPD and eventually function independent of assisted ventilation and supplemental oxygen if conditions for growth are optimized. Nevertheless, a relatively small proportion of the infants who develop BPD will go on to require prolonged ventilation. As noted previously, the collective use of steroids, surfactant replacement, and fewer traumatic ventilatory strategies has contributed to improved outcomes seen in infants with BPD. Thus far, it appears that the best prevention of BPD is the ability to avoid prematurity, lung barotrauma, overuse of the ventilator, and the release of free oxygen radicals associated with the inflammatory process. The decrease in barotrauma to the lungs is in large part due to the introduction of gentler methods of mechanical ventilation and the use of lower tidal volumes.32
Neurologic Sequelae in Neonates with Chronic Lung Disease
Premature infants with chronic lung disease are at risk for adverse neurologic outcomes because of the exposure to hypoxic events and because of central nervous system immaturity. Together, these pathophysiologic processes may result in a number of impairments and put them at risk for having neurodevelopmental disabilities.16,27,33 The smaller and more preterm the infant, the greater this risk is.
The two major types of brain injuries characteristic of premature infants are intraventricular hemorrhage (IVH) and periventricular leukomalacia (PVL). Intraventricular hemorrhage results from hemorrhaging into the delicate germinal matrix tissues—a fragile vascular bed seen in the developing brain. These delicate blood vessels are thought to be especially vulnerable to alterations in cerebral blood flow.34 The incidence of IVH is greatest in infants of lower gestational age; however, regardless of gestational age, the greatest risk period for IVH is in the first 3 to 4 postnatal days. IVH is diagnosed using cranial ultrasonography and is classified from grade I through IV according to severity: Grade I is a germinal matrix bleed only and a grade IV signifies parenchymal involvement of the hemorrhage with accompanying ventricular enlargement.34 Infants with the most severe IVH (grade IV) are at high risk for neurodevelopmental disabilities; however, recent data suggest that those with less severe involvement still may have learning difficulties.35,36
Periventricular leukomalacia is the major hypoxic brain injury seen in preterm infants and results in necrosis of the periventricular white matter. It generally occurs after the first week of life and is diagnosed using cranial ultrasonography. The evolution of PVL is of critical importance for its diagnostic and prognostic usefulness. The pathophysiologic mechanisms underlying this lesion continue to be investigated but are thought to be due to several factors. Traditionally it was thought that these lesions occurred in the arterial watershed zones due to the loss of cerebral autoregulation following an asphyxic event.34 More recent evidence suggests that the white matter damage may be the result of systemic inflammatory responses in the absence of adequate neuroprotective factors.34,37 Evidence also exists suggesting that the immature oligodendrocytes are metabolically vulnerable, thus making them susceptible to excitotoxicity.37
Persistent Pulmonary Hypertension and Meconium Aspiration Syndrome
As described earlier in the chapter, within the first few breaths, the vascular tone in the pulmonary circulation decreases, reducing the pressures on the right side of the heart. The foramen ovale closes functionally, followed within hours by functional closure of the ductus arteriosus; both of these structures undergo complete anatomic closure at a later time. Thus, normal postnatal circulation is established.
In PPH, pulmonary vasoconstriction occurs shortly after birth and results in extrapulmonary shunting of blood from the right to left side via the foramen ovale and/or ductus arteriosus. In addition to the increased pressures on the right side of the heart, the decreased flow through the lungs results in central hypoxemia and cyanosis that are not responsive to high concentrations of inspired oxygen. In the case of Joshua, his arterial blood gases remained abnormal in the presence of 100% oxygen, indicating that the inspired oxygen was not being picked up by the systemic circulation. The accepted clinical criteria for PPH are a PaO2 of less than 70 torr in and FiO2 of 1.0, absence of structural heart disease, and documented right to left shunting38; thus, it is essential to rule out congenital heart disease in an infant who is unresponsive to inspired oxygen.
Often associated with disorders of circulation or cord complications is meconium aspiration syndrome. MAS is defined by the presence of meconium below the vocal cords and occurs in up to 20% to 30% of infants with meconium stained amniotic fluid.39 The development of the syndrome is thought to be due to airway obstruction, chemical injury to the respiratory epithelium, and a secondary surfactant deficiency due to its inactivation by the meconium.40–42In approximately 7% to 20% of all deliveries, meconium is passed in the amniotic fluid.39,42 This phenomenon is rare before 34 weeks of age, and the risk of occurrence increases in relation to advanced gestation, with the greatest risk beyond 37 weeks’ gestational age.
Infants born through meconium-stained fluid face a 100-fold risk of developing respiratory distress compared to infants born through clear amniotic fluid. The risks of morbidity and mortality also differ with respect to the timing and the quality of the meconium. Typically, the consistency of meconium is described as being thick or thin. The presence of meconium at the onset of labor indicates that some event occurred prenatally; meconium that is present during labor is indicative of a more acute event. There is a five- to seven fold increased risk of death when thick meconium is present at the onset of labor.
A strong association exists between MAS and PPH for reasons that are not completely understood. Whether and to what extent the aspiration occurs in utero as opposed to during delivery has not been resolved. Furthermore, there are debates as to whether MAS represents chronic hypoxia in utero or whether the aspiration sets up a sequence of events that directly result in acute distress. If the infant has suffered in utero hypoxia and hypercapnia, they are more likely to develop PPH. As well, both of those conditions can stimulate fetal gasping and meconium passage, in which case the aspiration occurs before the birthing process. In these infants, there is a greater likelihood of having more serious and long-term respiratory and neurologic complications.39
Early management of the infant with PPH and MAS is focused on clearance of the meconium from the pharynx, trachea, and stomach, after which treatment is directed toward management of the acute distress. Strategies are typically directed at mechanical ventilation, circulatory support, and pulmonary arteriole vasodilation. The repertoire of treatment for PPH includes conventional therapies such as mechanical ventilation (to produce hyperoxia and hypocapnia), sedation, paralysis, alkali infusion, intravascular volume support, and normalization of serum electrolytes and glucose.38,43,44 Despite often aggressive management of babies with PPH, the diagnosis was associated with high rates of mortality prior to the development and use of extracorporeal membranous oxygenation (ECMO) in the mid-1980s.45 Currently ECMO is used as a rescue therapy of last resort in infants with PPH38,46 (see Fig. 21-3). In addition, more recent treatment strategies that are widely available include inhaled nitric oxide, high-frequency mechanical ventilation, and exogenous surfactant administration.47
FIGURE 21-3 Infant in neonatal intensive care unit. Note the presence of the extracorporeal membranous oxygenation (ECMO) system.
Inhaled nitric oxide is the newest of the aforementioned therapies and has been the subject of several clinical trials, because it was found to be a potent selective pulmonary vasodilator in both animals and patients with pulmonary hypertension. Prior to this, it had been difficult to obtain pulmonary vasodilation without widespread systemic hypotension.48 To date, clinical trials have demonstrated its efficacy in improving oxygenation and reducing the need for ECMO in babies with PPH.46 However, the optimal dose and timing of administration have yet to be agreed on, and it is not overwhelmingly clear whether the clinical improvements are always sustained long enough to reduce overall mortality.18 Recent studies have shown that the effects of inhaled NO are enhanced when used in conjunction with high-frequency oscillatory ventilation (HFOV).19,38,46
Although PPH is a transient condition, it can have devastating consequences and long-term effects if the lung tissue is injured or if there is brain injury from the postnatal asphyxia. If severe enough, the result could be hypoxic-ischemic encephalopathy (HIE). Through various mechanisms, the brain undergoes metabolic and vascular changes in response to the oxygen deprivation and decreased perfusion. Tissue damage may also result from the excitotoxic cascade (due to extracellular glutamate accumulation) and the release of oxygen-free radicals. Whereas all regions of the brain are susceptible, the watershed regions of the cerebral vasculature are particularly vulnerable to the hypoxia-ischemia. Differential patterns of lesions occur in preterm (see previous discussion of PVL) and full-term infants due to the location of these watershed zones. In the full-term infant, these regions are at the base of the cortical sulci. As well, these babies also seem to be vulnerable to deep gray matter injury, which is associated with a poor outcome.49
Summary of Risk Factors
Despite the significant advances in the care of medically fragile preterm and full-term infants, these babies, like Sara and Joshua, still face an increased risk of neurologic and/or developmental impairments and disability. Regardless of the diagnosis, these infants typically experience a prolonged period of hospitalization, have limited endurance secondary to cardiopulmonary compromise, and are often constrained with technical support—all of which limit their opportunities for movement. Essentially these babies are products of a deprived environment in which the opportunities for experience and action are quite limited. Not only does this impact their motoric competencies, but also it severely limits their ability to attach meaning and relevance to their environment, a critical feature of early sensorimotor development. The result of such deprivation may lead to a documented developmental delay for reasons that may not necessarily be explained by an organic or pathophysiologic mechanism; however, for many there are known neurologic impairments associated with their primary pathology. For these reasons, physical therapy management of these patients should ideally focus on the infant’s medical as well as on the developmental goals.
THRESHOLD BEHAVIORS
At this point, there is a lack of identified threshold behaviors shown to be useful predictors of physical therapy outcomes with this patient group. Patients who fall into Practice Pattern G are distinguished from those in other cardiopulmonary practice patterns essentially by virtue of their age. In this pattern, the patients are neonates—which, by formal definition is an infant who is 0 to 4 weeks of age—although the practice pattern extends the age group to 4 months. By virtue of their immaturity, these patients have unique characteristics that make them especially vulnerable to failure of the respiratory pump and to impaired gas exchange. As a group, infants who are high risk and medically fragile are overrepresented in the population of children who end up having neurodevelopmental impairments and disabilities. Thus, in a best-practice setting, physical therapy management would include strategies to address the acute medical issues as well as strategies to address the neurodevelopmental consequences that the infant is or may be at risk for.
The most widely accepted framework for working with these vulnerable infants utilizes an individualized approach to care.12,50,51 By observing each infant’s behavioral and physiologic responses to interaction, an individualized care plan incorporates knowledge of the infant’s stressors and thus limits unnecessary stimulation. This approach to care of infants in the NICU has been shown to have a number of positive effects such as a lower incidence of intraventricular bleeds, less severe chronic lung disease (less time on the ventilator, decreased need for supplemental oxygen), faster weight gain, and shorter hospital stays.14,15 What is not known, however, are those critical behaviors or measures that can be of predictive or of prognostic value to physical therapy outcomes. Most would agree that there is paucity of such research and of studies that meet the rigorous criteria of best evidence.
LIMITS OF OUR KNOWLEDGE
It is well known that the human is capable of growth, repair, and regeneration in a number of systems. The last stage of lung development, for example, continues well into childhood. Over 90% of the alveoli develop postnatally. For infants with chronic lung disease, this allows much of their growth and healing to occur with potentially new and healthier lung tissue. In the central nervous system, there are also developmental changes in neuronal structure and function that occur postnatally. Recently there has been evidence from several studies demonstrating neuronal and functional plasticity in the central nervous system following damage.
These are but a few examples which highlight the capabilities of the human body. Our limits, as a profession, lie in our ability to exploit these “windows of opportunity” that exist and to better define how we can impact recovery and prevent secondary problems. Although there has been research examining different issues with respect to physical therapy evaluation and/or intervention with high-risk infants, to date, there is not strong evidence of its effectiveness in reducing or ameliorating the adverse pulmonary or neurodevelopmental impairments often seen in high-risk infants. The environment is ripe for our profession to lead the way in asking and answering the critical questions regarding the efficacy of our interventions.
In this group of patients, we have a unique opportunity to impact on their development almost from the beginning. The critical question though is, “Do we?” Does physical therapy intervention with neonates improve their cardiopulmonary status? Does a developmentally appropriate, functional movement program increase their “exercise” tolerance? What are the parameters for exercise training in a neonate? What is the cost–benefit ratio of exercise in an infant with chronic lung disease? What are the long-term effects of early intervention? How “early” is too early? The answers to these, and many other questions, are long overdue. Our challenge now and in the future will be to better define our roles and the expected outcomes in our care of high-risk neonates.
NAGI MODEL
The disablement associated with respiratory failure in the neonate is outlined in Table 21-12. The two primary pathologies under which secondary pathologies, impairments, functional limitations, and disabilities fall are bronchopulmonary dysplasia and persistent pulmonary hypertension with meconium aspiration syndrome. Note that, even as a neonate, this child may be destined to develop disabilities related to parental bonding and developmental delays. Aggressive, early physical therapy interventions aimed at correcting impairments and functional limitations will hopefully minimize disabilities of the neonate in respiratory failure.
TABLE 21-12 The Nagi Model Applied to Respiratory Failure in the Neonate
REFERENCES
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2.Moore KL, Persaud TVN. The Developing Human: Clinically Oriented Embyrology. Philadelphia, PA: WB Saunders; 1998.
3.Gluckman PD, Harding JE. Fetal growth retardation: underlying endocrine mechanisms and postnatal consequences. Acta Paediatrica Suppl. 1997;422:69-72.
4.Lee K, Khoshnood B, Wall SN, et al. Trend in mortality from respiratory distress syndrome in the United States, 1970–1995. J Pediatr. 1999;134:434-440.
5.Gluckman PD, Sizonenko SV, Bassett NS. The transition from fetus to neonate—an endocrine perspective. Acta Pediatr Suppl. 1999;428:7-11.
6.Apgar V. Proposal for a new method of evaluation of newborn infants. Curr Res Anesth Analg. 1953;32:260-267.
7.Kotecha S. Lung growth: implications for the newborn infant. Arch Dis Child Fetal Neonat Ed. 2000;82(1):F69-F74.
8.Crane LD. Physical therapy for the neonate with respiratory disease. In: Irwin S, Tecklin JS, eds. Cardiopulmonary Physical Therapy. St Louis, MO: Mosby; 1995:486-515.
9.Oberwaldner B. Physiotherapy for airway clearance in paediatrics. Eur Respir J. 2000;15:196-204.
10.Kornecki A, Frndova H, Coates AL, Shemie SD. A randomized trial of prolonged positioning in children with acute respiratory failure. Chest. 2001;119(1):211-218.
11.Sweeney JK, Heriza CB, Reilly MA, et al. Practice guidelines for the physical therapist in the neonatal intensive care unit. Pediatr Phys Ther. 1999;11:119-132.
12.Als H. A synactive model of neonatal behavioral organization: framework for the assessment of neurobehavioral development in the premature infant and for support of infants and parents in the neonatal intensive care environment. Phys Occupat Ther Pediatr. 1986;6(3/4):3-54.
13.Sweeney JK. Physiologic adaptation of neonates to neurologic assessment. Phys Occupat Ther Pediatr. 1986;6:155-169.
14.Als H, Lawhon G, Duffy FH, et al. Individualized developmental care for the very low birthweight preterm infant: medical and neurofunctional effects. JAMA. 1994;272:853-858.
15.Als H, Lawhon G, Brown E, et al. Individualized behavioral and environmental care for the very low birth weight preterm infant at risk for bronchopulmonary dysplasia: neonatal intensive care unit and developmental outcome. Pediatrics. 1986;76:1123-1132.
16.Campbell SK. The infant at risk for developmental disability. In: Campbell SK, ed. Decision Making in Pediatric Neurologic Physical Therapy. New York: Churchill Livingstone; 1999:260-332.
17.Einspieler C, Prechtl HFR, Ferrari F, et al. The qualitative asessment of general movements in preterm, term and young infants-review of the methodology. Early Hum Dev. 1997;50(1): 47-60.
18.Cheifetz IM. Inhaled nitric oxide: plenty of data, no consensus. Crit Care Med. 2000;28(3):902-903.
19.Kinsella JP, Abman SH. Clinical approach to inhaled nitric oxide therapy in the newborn with hypoxemia. J Pediatr. 2000;136(6): 717-726.
20.Watchko JF, Mayock DE, Standaert TA, Woodrum DE. The ventilatory pump: neonatal and developmental issues. Adv Pediatr. 1991;38:109-134.
21.Bureau MA, Begin R. Chest wall diseases and dysfunction in children. In: Kendig EL, Chernick V, eds. Disorders of the Respiratory Tract in Children. Philadelphia, PA: WB Saunders; 1983: 601-616.
22.Pagtakhan RD, Chernick V. Intensive care for respiratory disorders. In: Kendig EL, Chernick V, eds. Disorders of the Respiratory Tract in Children. 4th ed. Philadelphia, PA: WB Saunders; 1983:145-168.
23.Make BJ, Hill NS, Goldberg AI, et al. Mechanical ventilation beyond the intensive care unit: report of a Consensus Conference of the American College of Chest Physicians. Chest. 1998;113(5):289S-344S.
24.Halliday HL, Ehrenkranz RA. Early (<96 hours) postnatal corticosteroids for preventing chronic lung disease in preterm infants. Cochrane Database Syst Rev. 2000;(2):CD001146. http://www.ncbi.nlm.nih.gov/pubmed/10796252?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=11. Accessed January 1, 2010.
25.Rennie JM, Bokhari SA. Recent advances in neonatology. Arch Dis Child. 1999;81(1):1F-4F.
26.Gortner L, Wauer RR, Hammer H, et al. Early versus late surfactant treatment in preterm infants of 27 to 32 weeks’ gestational age: a multicenter controlled clinical trail. Am Acad Pediatr. 1998;102:1153-1160.
27.Bancalari E. Changes in the pathogenesis and prevention of chronic lung disease of prematurity. Am J Perinatol. 2001;18:1-9.
28.Northway WH Jr, Rosan RC, Porter DY. Pulmonary disease following respirator therapy of hyaline-membrane disease. Bronchopulmonary dysplasia. N Engl J Med. 1967;276:357-368.
29.Jobe AH, Bancalari E. Bronchopulmonary dysplasia. Am J Respir Crit Care Med. 2001;163:1723-1729.
30.Eber E, Zach MS. Long term sequelae of bronchopulmonary dysplasia (chronic lung disease of infancy). Thorax. 2001;56:317-323.
31.Husain NA, Siddiqui NH, Stocker JR. Pathology of arrested acinar development in postsurfactant bronchopulmonary dysplasia. Hum Pathol. 1998;29:710-717.
32.Thome UH, Carlo WA. High frequency ventilation in neonates. Am J Perinatol. 2000;17(1):1-9.
33.Bregman J, Farrell EE. Neurodevelopmental outcome in infants with bronchopulmonary dysplasia. Clin Perinatol. 1992;19(3): 673-694.
34.Ment LR, Schneider KC, Ainley MA, Allan WC. Adaptive mechanisms of the developing brain. Clin Perinatol. 2000;27(2):303-323.
35.Ment LR, Vohr B, Allan W, et al. Outcome of children in the indomethacin intraventricular hemorrhage prevention trial. Am Acad Pediatr. 2000;105:485-491.
36.Whitaker AH, Feldman JF, Van Rossem R, Schonfeld IS, et al. Neonatal cranial ultrasound abnormalities in low birth weight infants: relation to cognitive outcomes at six years of age. Pediatrics. 1996;98(1):719-729.
37.Dammann O, Leviton A. Brain damage in preterm newborns: biological response modification as a strategy to reduce disabilities. J Pediatr. 2000;136(4):433-438.
38.Gross I. Recent advances in respiratory care of the term neonate. Ann NY Acad Sci. 2000;900:151-158.
39.Klingner MC, Kruse J. Meconium aspiration syndrome: pathophysiology and prevention. J Am Board Fam Pract. 1999;12(6): 450-466.
40.Meydanli MM, Dilbaz B, Caliskan S, Dilbaz AH. Risk factors for meconium aspiration syndrome in infants born through thick meconium. Int J Gynaecol Obstet. 2001 Jan;72(1):9-15.
41.Lotze A, Mitchell BR, Bulas DI, et al. Multicenter study of surfactant (beractant) use in the treatment of term infants with severe respiratory failure. J Pediatr. 1998;132(1):40-47.
42.Soll RF, Dargaville P. Surfactant for meconium aspiration syndrome in full term infants. Cochrane Database System Rev. 2000;4.
43.Paz Y, Solt I, Zimmer EZ. Variables associated with meconium aspiration syndrome in labors with thick meconium. Eur J Obstetr Gynecol Reproduct Biol. 2000;94:27-30.
44.Walsh-Sukys MC, Tyson JE, Wright LL, et al. Persistent pulmonary hypertension of the newborn in the era before nitric oxide: practice variation and outcome. Pediatrics. 2000;105(1): 14-20.
45.Hintz SR, Suttner DM, Sheehan AM, et al. Decreased use of neonatal ECMO: how new treatment modalities have affected ECMO utilization. Pediatrics. 2000;106(6):1339-1343.
46.Lemons JA, Blackmon LR, Kanto WP, et al. Use of inhaled nitric oxide. Pediatrics. 2000;106(2):344.
47.Christou H, Van Marter LJ, Wessel DL, et al. Inhaled nitric oxide reduces the need for extracorporeal membrane oxygenation in infants with persistent pulmonary hypertension of the newborn. Crit Care Med. 2000;28(11):3722-3727.
48.Cornfield DN, Maynard RC, deRegnier RA, Guiang SF, et al. Randomized, controlled trial of low-dose inhaled nitric oxide in the treatment of term and near-term infants with respiratory failure and pulmonary hypertension. Pediatrics. 1999;104(5): 1089-1094.
49.Roland EH, Poskitt K, Rodriguez E, et al. Perinatal hypoxicischemic thalamic injury: clinical features and neuroimaging. Ann Neurol. 1998;44:161.
50.Als H, Lester BM, Tronick EZ, Brazelton TB. Toward a research instrument for the assessment of preterm infant’s behavior (APIB). In: Fitzgerald HE, Lester BM, Yogman, eds. Theory and Research in Behavioral Pediatrics. New York: Plenum; 1982:63-65.
51.Lotas MJ, Walden M. Individualized developmental care for very low birth weight infants: a critical review. JOGNN. 1996;25: 681-687.
CHAPTER 21
An International Perspective: Colombia—Physical Therapy Practice in Neonates from the Colombian Perspective
Adriana Yolanda Campos, Maria Fernanda Guzman, Edgar Debray Hernandez, & Gloria Amalfi Luna
Physical therapy in Colombia is considered a liberal arts profession within the area of human health. University training is required with emphasis on patient care in relation to his/her family and the community in which they develop. The objective of physical therapy practice is the study, understanding, and management of human physical movement—considered an essential element that contributes to optimun health. Physical therapy in Colombia is directed toward the maintenance and optimization of movement as well as prevention of, and recovery from, accidental injury. The habilitation and rehabilitation of patients is included with the purpose of optimizing the quality of life and of contributing to the social development of individuals. The foundation of physical therapy practice is knowledge of biological, social, and humanistic sciences, which are used to advance the profession’s own theories and technologies (Law 528 of 1999).
Colombian physical therapists receive training in the conduction of scientific research and in strategies related to health and kinetic well-being. Physical therapists are also trained in health care policy and management, and in academic endeavors.
Presently, there are 26 physical therapy programs offering pregraduation university training in Colombia. In addition, there are six specialization programs in physical therapy—four of them related to the cardiopulmonary field.
In Colombia, provision of physiotherapy services to the neonate population is based on an integrated process recognizing normal human body motions called HBM. This approach requires measurements and assessments that are individuated to the patient. The results of these assessments can be used to categorize the neonate based on the complexity of their nonsystemic interactions. Intervention strategies can then be implemented which will facilitate proper neonatal development. Appropriate interventions usually include motor activities, which are graduated from lowest to highest complexity. Those at the lowest level include activities designed to enhance force development, flexibility, speed, and cardiovascular endurance. The next level is perceptive motor activities, which include coordination. Coordination is subdivided into issues of equilibrium, perception, kinetics, and perceptions of time and space. Finally, resultant activities are at the highest level of complexity and include skills that require speed and agility.
A properly planned and executed physiotherapy assessment establishes the extent of involvement of the neonate while under stress and provides information on the real or possible impact that such findings may have on the future development of normal MCH.
At the Corporacion Universitaria Iberoamericana in Bogota, our neonatal assessment has three components: the anatomical status, the physiological status, and the motor status. The anatomical status is dependent on the biotype of morphological features of the neonate—its size, weight, cephalic and thoracic measurements, facial symmetry, skin condition (eg, vernix, color nails, lanugo), and gestational age.1,2 The physiological status includes assessment of the current and potential capacity of the cardiovascular and pulmonary systems, both at rest and under stress. These tests include measurements of oxygen consumption, the anaerobic threshold, and the aerobic functional capacity. The motor status is understood to mean the set of attributes that are relevant to age-appropriate MCH and that are not necessarily dependent on the cardiovascular system. The purpose of such measurements is to determine the extent of neurophysiologic maturity of the neonate and his or her adaptability to the environment. Such adaptability is particularly important for the neonate, as it passes from a wet, warm, and dark environment to one that is cold, luminous, and noisy. It is this dramatic change that forces the newborn to develop adaptive psychophysiological responses as it struggles for survival.
At our institution, the physiotherapist would begin the plan of care with a thorough review of the clinical record in order to identify factors that may influence neonatal development. The therapist selects and applies appropriate tests that are then used to determine the maturity of sensory receptors and motor pathways.
•Sensory organs. It must be emphasized that high-risk neonates do not show sufficient neuroanatomic development and maturity for optimal kinetic function. It is essential that the physiotherapist establish the functionality of these elements, especially because they are the fundamental pillars upon which human kinetic diversity is built.
•Motor activity. This includes both involuntary and voluntary activity. Involuntary motor activity involves assessment of muscle tone and reflex development. Voluntary activity refers to the ability of the neonate to initiate spontaneous movement. It is particularly important to note the neonate’s posture as a reflection of possible injury to the neuromuscular system.
Deterioration of functional aerobic capacity is one of the most common problems observed in neonates, particularly in preterm neonates. These individuals are particularly susceptible to functional aerobic impairments because of the lack of maturity of the cardiovascular and pulmonary systems, which render them maladaptive to a hostile and constantly changing environment. Cardiac pathologies observed among neonates in Columbia include cardiac pump dysfunction and failure. Pulmonary pathologies include both restrictive (eg, hyaline membrane disease) and obstructive phenomena (eg, bronchopulmonary dysplasia).
Identification of deficiencies in the cardiovascular and pulmonary systems allows the physiotherapist to link these systems to physical motor quality. This is accomplished by filling in data to the following assessment categories:
•Gas exchange, assessed through indexes of oxygenation (eg, PaO2, SaO2, PaO2/FiO2, shunt, interalia) and indexes of ventilation (PaCO2, PetCO2)
•Ventilation mechanics, assessed through calculations of distension of pulmonary parenchyma and/or thorax, strength to flux in the airway, and the qualitative analysis (and if possible, the quantitative analysis) of respiratory load
•Hydroelectrolytic balance
•Acid–base balance
•Cardiac pump function, assessed through indirect inferences from calculations of preload, afterload, contractility, and chronotropy
•Tissue perfusion, assessed through clinical observation, or through the derivation of data from calculations of the a- 
O2 difference and/or the rate of oxygen withdrawal
•Fluid input/consumption ratio
Using data obtained from tests and measures, and from direct observations of the neonate, the physiotherapist can determine a plan of care. The patient’s current physical status will determine the appropriateness of interventions, goals, and therapeutic modes designed to enhance cardiovascular and pulmonary functions and promote kinetic development.
Therapeutic strategies that can improve and/or reverse pulmonary dysfunction range from position changes and oxygen supplementation to the use of ventilatory support (invasive or noninvasive) aimed at optimizing gaseous exchange and ventilation.
In Colombia, stimulation that is provided to the at-risk neonate usually takes the form of a set of interventions aimed at providing the neonate with experiences that stimulate body receptors from the time of birth in order to maximize kinetic potential. Thus, both sensory and motor stimuli are presented to the neonate during any given treatment session.3
Whether the stimuli are sensory or motor, the goal of treatment is to release motor responses. This approach provides the rationale for the use of tactile stimuli to release sucking or searching responses, the use of position changes to encourage physiological stability, and the stimulation of vestibular and kinetic receptors that will promote the development of basic motor patterns.4
REFERENCES
1.Cruz I. Guia del Manejo Fisioterapeutico Para la Atencion del Recien Nacido con Enfermedad de Membrana Hialina Grado II. 2000.
2.Manno R. Fundamentos Del Entrenamiento Deportivo. Barcelona, Spain: Paidotribo; 1994.
3.Correa A. Recien Nacido Normal. Medellin, Colombia: OID; 1997.
4.Diaz P. Estimulacion Temprana. Lidium: Buenos Aires; 1990.