MIMS COLLEGE OF NURSING PUTHUKODE

HIGH RISK NEWBORN

TERM PAPER ON HIGH RISK NEWBORN

PREPARED BY:
ASHA JOSE, 1ST YEAR M. Sc NURSING, (PEDIATRIC NURSING) MIMS CON, CALICUT.

SUBMITTED ON: 10-09-2012.

INDEX SL NO. 1 CONTENT HIGH RISK NEWBORN

DEFINITION CLASSIFICATION FACTORS ASSOCIATED WITH HIGH RISK NEWBORN

PAGE NO. 1

2 3

PRETERM BABY COMMON RESPIRATORY SYSTEM ABNORMALITIES IN HIGH RISK NEWBORN

EMBRYONIC DEVELOPMENT OF THE RESPIRATORY SYSTEM APNEA OF PREMATURITY PERINATAL ASPHYXIA

8-11

12-15 15-19 19-34 29 31 35-40 40-46 47-49 49-51 52-66 67-69 70-79 80-84 84 84-85.

Neonatal resuscitation ECMO

MECONIUM ASPIRATION SYNDROME RESPIRATORY DISTRESS SYNDROME BRONCHOPULMONARY DYSPLACIA

4 5 6 7 8 9 10

REETINOPATHY OF PREMATURITY NNHB NECROTISING ENTEROCOLITIS NEONATAL SEIZURE NURSING CARE CONCLUSION REFERENCE

HIGH RISK NEWBORN

DEFINITION: A baby born with an increased risk for maintaining life like normal either due to prematurity or post maturity or due to multiple factors leading to risk for life due to maternal factors, fetal factors or environmental factors. The high risk neonate can be defined as a newborn, regardless of gestational age or birth weight, who has a greater than average chance of morbidity or mortality because of conditions or circumstances superimposed on the normal course of events associated with birth and the adjustment to extra uterine existence. CLASSIFICATION According to size According to gestational age According to mortality According to size: LBW* Moderate LBW babies VLBW * Extremely LBW AGA * SGA * IUGR* LGA* : birth weight less than 2500 g regardless of gestational age : birth weight is 1501-2550 g. : birth weight less than 1500 g : birth weight less than 1000 g : birth weight between 10th percentile on intrauterine growth curves. : birth weight falls below 10th percentile on growth curves. : SGA and retarded intrauterine growth. : birth weight falls above 90th percentile on growth chart. LBW VLBW AGA SGA IUGR LGA According to gestational age,
4

Low Birth Weight - Very Low Birth Weight - Appropriate for Gestational Age - Small for Gestational Age. - Intra Uterine Growth Retardation - Large for Gestational Age.

Premature (preterm) babies : born before 37 completed weeks of gestation. Full term babies According to Mortality. Live Birth Fetal death Neonatal death : neonate manifests heart beat, breaths or displays voluntary movement. : death of fetus after 20th week of gestation, absence of signs of life after birth. : death of newborn occurs in the first 27 days of life. Early neonatal death- occurs in first week of life. Late neonatal death occurs at 7-27 days. Perinatal Mortality : total number of fetal and early neonatal death per 1000 live births. Postnatal Death : death occurs between 28 days and one year. : born between beginning of 38th and completion of 42nd week.

FACTORS ASSOCIATED WITH HIGH RISK NEWBORN A) Maternal characteristics and associated risk for fetus and neonate. 1. Age at delivery: Over 40 years: chromosomal abnormalities, macrosomia, IUGR, blood loss. Under 16 years: IUGR, prematurity, child abuse/neglect. 2. Personal factors. Poverty: prematurity, infection, IUGR. Drug/alcohol use: Drug use, fetal alcohol syndrome, sudden infant death syndrome, child abuse/neglect. Poor diet: mild IUGR to fetal demise. Trauma: abruption placentae, fetal demise, prematurity. 3. Maternal medical conditions and associated risk for fetus or neonate. Diabetes Mellitus: congenital anomalies, still birth, respiratory distress, hypoglycemia, birth injury. Thyroid disease: Goiter, hypothyroidism, hyperthyroidism. Renal disease: IUGR, still birth, prematurity. UTI: prematurity, sepsis. Heart, lung disease. Hypertension. Anemia: IUGR, still birth, asphyxia, prematurity, hydrops. Isoimmunisation: still birth, anemia, jaundice, and hydrops. Thrombocytopenia: still birth, bleeding. 4. Obstetric history and associated risk for fetus or neonate. Past history of infant with prematurity, jaundice, RDS.
5

 B) 1. 2. 3. 4. 5. 6. 7.

Maternal medications. Bleeding in early pregnancy: still birth, prematurity. Hyperthermia: fetal demise, fetal anomalies. Bleeding in third trimester: still birth, anemia. Premature rupture of membrane: infection, sepsis. TORCH infections. Trauma: fetal demise, prematurity.

Fetal conditions and associated risk for fetus or neonate. Multiple gestation: prematurity, IUGR, asphyxia, birth trauma. IUGR: fetal demise, congenital anomalies. Macrosomia: congenital anomalies, birth trauma, hypoglycemia. Abnormal fetal presentation or position. Abnormality of fetal heart rate or rhythm: hydrops, asphyxia, CHF. Decreased activity: fetal demise, asphyxia. Polyhydramnios: anencephaly, other CNS disorders, problem with swallowing (agnathia, esophageal atresia), diaphragmatic hernia, intrauterine infection, inability to concentrate urine, maternal diabetes. 8. Oligohydramnios: IUGR, placental insufficiency, post maturity, fetal demise, intrapartum distress, renal agenesis.

C) Conditions of labor and delivery and associated risk for fetus or neonate. 1. Premature labor: RDS, other issues of prematurity. 2. Post term labor: still birth, asphyxia, meconium aspiration. 3. Maternal fever: infection, sepsis. 4. Maternal hypotension: still birth, asphyxia. 5. Rapid labor: birth trauma, ICH, retained fetal lung fluid. 6. Prolonged labor: still birth, asphyxia, birth trauma. 7. Abnormal presentation: birth trauma, asphyxia. 8. Uterine tetany. 9. Meconium stained amniotic fluid: still birth, asphyxia, meconium aspiration syndrome. 10. Prolapsed cord. 11. Caesarean section: RDS, retained fetal lung fluid/ transient tachypnea. 12. Obstetric analgesia and anesthesia: respiratory depression, hypotension, hypothermia. 13. Placental anomalies: Small placenta- IUGR. Large placenta- hydrops, maternal diabetes, large infant. Torn placenta and/or umbilical vessels: blood loss. Abnormal attachment of vessels to placenta: blood loss. D) Immediately evident neonatal conditions and associated risk for fetus or neonate. 1. Prematurity: RDS
6

2. 3. 4. 5. 6. 7.

Low 5 minute apgar score Low 15 minute apgar score. Pallor or shock: blood loss Foul smell of amniotic fluid or membranes: infection. Small size for gestational age. Post maturity.

PREMATURE OR PRETERM BABY

INTRODUCTION Preterm birth refers to the birth of a baby before the developing organs are mature enough to allow normal postnatal survival. Premature infants are at greater risk for short and long term complications, including disabilities and impediments in growth and mental development. Significant progress has been made in the care of premature infants, but not in reducing the prevalence of preterm birth. Preterm birth is among the top causes of death in infants worldwide. They may have health problems because their organs did not have enough time to develop. Preemies need special medical care in a neonatal intensive care unit, or NICU. DEFINITION A baby born before 37 completed weeks of gestation calculating from the first day of last menstrual period is defined as preterm baby. INCIDENCE Preterm baby constitutes two- third of low birth weight babies. Incidence is 30-40% in developing countries. ETIOLOGY Unknown in most cases. Predisposing factors include: Low socio economic status.

Maternal factors Maternal age: younger than 16 or older than 35.

8

Maternal activity requiring long periods of standing or substantial amount. Malnutrition. Chronic diseases such as heart, renal or diabetes.

Obstetric factors such as uterine malformations, uterine trauma, placenta previa etc. Fetal conditions such as IUGR or severe hydrops may require preterm delivery. CLINICAL EVALUATION Weight: 2500g or less. Length: less than 44cm. Posture: the preterm infant lies in a relaxed attitude, limbs more extended; the body size is small, the head may appear somewhat larger in proportion to the body size. Head: skull bones are soft with wide sutures. Head circumference disproportionally exceeds that of chest. Ear: cartilages poorly developed. Ear may fold easily. Hair: fine, feathery; lanugo cover the back and face. Sole: sole of the foot may appear more turgid and may have only fine wrinkles. Female genitalia: clitoris prominent, labia majora poorly developed. Male genitalia: scrotum undeveloped, minimal rugae, testes may be in the inguinal canal or in the abdominal cavity. Scarf sign: the preterm infants elbow may be easily brought across the chest with little or no resistance. Term infants resist the attempt to bring the elbow past the mid line. Grasp reflex: weak. Heel-to-ear maneuver: heel is easily brought to the ear. PROBLEMS OF PREMATURITY Respiratory system : Perinatal depression, RDS due to surfactant deficiency, Apnea, Broncho pulmonary dysplasia (BPD).
9

Neurologic neuronal injury.

: Perinatal depression, ICH, Periventricular white matter and other

Cardio vascular : hypotension due to hypovolemia, cardiac dysfunction, vasodilation due to sepsis. PDA is common and will lead to Congestive heart failure. Hematologic Gastro intestinal : anemia, hyperbilirubinemia. : necrotizing enterocolitis.

Metabolic problems : in glucose and calcium metabolism Renal : low glomerular filtration rate.

Temperature regulation: premature infants are especially susceptible to hypo and hyperthermia. Immunologic Ophthalmologic the infants. MANAGEMENT Alert the intensive care nursery and implement a team approach.neonatologist, advanced practice nurse and a respiratory therapist should be present. If not require resuscitation, transfer immediately to a heated incubator or to NICU. Weigh the baby, start with IV fluids, oxygen therapy and other therapeutic interventions are initiated as needed. Temperature regulation Radiant warmer Mummification Kangaroo mother care. : greater risk of infection. : Retinopathy of Prematurity (ROP) may develop in the immature retina in

Maintain nutrition. Preventing infection Follow strict hand hygiene. Use hand rub before and after contact with the baby.

Restrict visitors. Fluid therapy

10

Modified Isolyte P = 10 ml 25%D + 40 ml Isolyte P. For babies weighing less than 1.5 kg, the type of fluid is 5%D for day 0 and 1; then Isolyte P is used from day 2 onwards.

Fluid requirement for preterm babies weighing more than 1.5 kG

Day

Fluid amount in ml/kg/day 80 100 120 140 150 150

Type of fluid

Day 0 day 1 day 2 day 3 day 4 day 5

10% D 10% D Modified Isolyte P M. Isolyte P M. Isolyte P M. Isolyte P

11

COMMON RESPIRATORY SYSTEM ABNORMALITIES IN HIGH RISK NEWBORNS EMBRYONIC DEVELOPMENT OF RESPIRATORY SYSTEM The respiratory system begins as a ventral outgrowth (laryngotracheal groove) from the wall of the foregut, close to the fourth and sixth pharyngeal pouches. The groove deepens and grows downwards to form a pouch-like evagination, fully open to the foregut. Two longitudinal folds of tissue (tracheo-oesophogeal folds) on either side of the groove grow together and fuse, forming a new tube (laryngeotracheal tube) distinct from the foregut. Communication with the foregut is maintained via a longitudinally oriented slit-like opening (laryngeal orifice). Proliferation of the underlying mesenchyme forms swellings around the laryngeal orifice (epiglotal swelling and arytenoid swellings) from which the epiglottis, glottis, laryngeal cartilages and musculature will develop. At the same time, the laryngeotracheal tube elongates downwards and penetrates the underlying splanchnopleuric mesoderm. A distinct swelling develops at the distal end and is termed the lung bud (respiratory diverticulum). Approximately 28 days after fertilisation, the lung bud branches to form the left and right primary bronchial buds, which will ultimately develop into the left and right lungs. Branching is in part directed by the interaction of the epithelium with the underlying splanchnic mesoderm. By the fifth week, elongation, branching and budding of the two bronchial buds gives rise to three bronchial stems on the right and two on the left - these are the foundation for the lobular organisation of the mature lung. Dichotomous branching continues for approximately ten weeks, establishing the conducting portion of the airways. Up to 24 orders of branches are generated, the final level being the prospective terminal bronchioles. New branches are being formed within a rapidly proliferating, homogeneous mesenchyme. Differentiation of the mesenchyme and epithelia begins in the more proximal regions of the airways and progresses distally, beginning during week 10 when mesenchymal cells condense around the larynx and trachea. These will form smooth muscle and supporting cartilages. The pulmonary arteries and veins develop in parallel with the conducting portion of the lungs and follow the same branching pattern.

12

Initially the airway lumina are very narrow, with a thick pseudostratified epithelial lining. From week 13 onward, the lumina enlarge and the epithelium thins to a more columnar structure. The pluripotent epithelial cells differentiate to cilliated cells and goblet cells, initially in the proximal regions of the developing lung and progressing distally. From weeks 16 to 24, the primordia of the respiratory portions of the lungs are formed. The terminal bronchioles divide to form two respiratory bronchioles which in turn branch to form 3 to 6 primitive alveolar ducts, ending in terminal sacs. At the same time, extensive angiogenesis within the peripheral mesenchyme leads to vascularisation of the developing respiratory structures. The cuboidal intermediate cells of the lower airways differentiate to form cilliated cells and clara cells. Peripheral mesenchymal cells differentiate to form the visceral pleura, the remaining mesenchymal cells gain the characteristics of stromal fibroblasts. By week 26, the terminal sacs have started to dilate, and will eventually differentiate into alveolar complexes. The stroma thins, bringing the growing capillary network into close association with the immature alveoli. The cuboidal cells of the terminal sac epithelium differentiate into alveolar type-II cells which secrete low levels of surfactant. Where cells with type-II phenotype juxtapose a capillary, they differentiate to type-I cells, which flatten and can provide a functional though inefficient blood/air barrier if the infant is born prematurely. During subsequent weeks there is a rapid expansion of the respiratory portion of the lung. Terminal saccules dilate and branch to form further generations of terminal saccules, vascularised septa form within growing terminal sacs and Type-I cells continue to flatten and spread, increasing the surface area available for gas exchange. The parenchyma of the lung continues to thin, and fibroblasts lay down the collagen and elastin fiber components of the stroma. The composition of pulmonary surfactant is developmentally regulated. By week 30, there is a significant rise in the amount of surfactant secreted from the type-II cells. By week 36, the stroma of the lung has thinned to the extent that capillaries may protrude into the prospective alveolar airspaces. The final stages of maturation of the respiratory system occur after 36 weeks gestation and continues into adulthood. At around 36 weeks, the first mature alveoli appear, characterised by thin walled interalveolar septa with a single layered capillary network. The diameter of the capillaries is sufficiently large that they may span the alveolar walls and interact with the
13

airspaces on both sides. New alveoli are generated by a process of septal subdivision of existing immature alveoli. There is a growth spurt soon after birth, though new alveoli continue to form at a high rate for up to 3 years. As the alveoli mature and the walls thin, there is a decrease in the relative proportion of stroma to total lung volume which contributes significantly to growth for 1 to 2 years after birth. By 3 years, the overall morphology of the lung has been established and subsequent expansion occurs through a proportional growth of all lung components until adulthood. Developmental Stages

Embryonic phase (3-7 weeks) Initial budding and branching of the lung buds from the primitive foregut. Ends with the development of the presumptive broncho-pulmonary segements.

Pseudoglandular phase (7-16) weeks. Further branching of the duct system (up to 21 further orders) generates the presumptive conducting portion of the respiratory system up to the level of the terminal bronchioles. At this time the future airways are narrow with little lumens and a pseudostratified squamous epithelium. They are embedded within a rapidly proliferating mesenchyme. The structure has a glandular appearance.

Canalicular phase (16-24) weeks The onset of this phase is marked by extensive angiogenisis within the mesenchyme that surrounds the more distal reaches of the embryonic respiratory system to form a dense capillary network. The diameter of the airways increases with a consequent decrease in epithelial thickness to a more cuboidal structure. The terminal bronchioles branch to form several orders of respiratory bronchioles. Differentiation of the mesenchyme progresses down the developing respiratory tree, giving rise to chondrocytes, fibroblasts and myoblasts.

Terminal sac phase (24-36) weeks Branching and growth of the terminal sacs or primitive alveolar ducts. Continued thinning of the stroma brings the capillaries into apposition with the prospective alveoli. Functional type-II pneumonocytes differentiate via several intermediate stages from pluripotent epithelial cells in the prospective alveoli. Type I pneumonocytes differentiate from cells with a type-II like phenotype. These cells then flatten, increasing the epithelial surface area by dilation of the saccules, giving rise to immature alveoli. By 26 weeks, a rudimentary though functional blood/gas barrier has formed. Maturation of the alveoli continues by further enlargement of the terminal sacs,
14

deposition of elastin foci and development of vascularised septae around these foci. The stroma continues to thin until the capillaries protrude into the alveolar spaces.

Alveolar phase (36 weeks - term/adult) Maturation of the lung indicated by the appearance of fully mature alveoli begins at 36 weeks, though new alveoli will continue to form for approximately three years. A decrease in the relative proportion of parenchyma to total lung volume still contributes significantly to growth for 1 to 2 years after birth, thereafter all components grow proportionately until adulthood.

APNEA OF PREMATURITY Apnea is breathing that slows down or stops from any cause. Apnea of prematurity refers to short episodes of stopped breathing in babies who were born before they were due. DEFINITION: Apnea of prematurity is defined as cessation of breathing by a premature infant that lasts for more than 15-20 seconds and/or is accompanied by hypoxia or bradycardia and color change. CAUSES: There are several reasons why newborns, especially premature babies, may have apnea, including:

Their brain is not fully developed The muscles that keep the airway open are weak

Other stresses in a sick or premature baby may worsen apnea, including:

Anemia, Feeding problems Heart or lung problems, Infection Low oxygen levels, Overstimulation, Temperature problems

TYPES: Apnea is traditionally classified as either : obstructive, central, or mixed.

Obstructive apnea may occur when the infant's neck is hyperflexed or conversely, hyperextended. It may also occur due to low pharyngeal muscle tone or to inflammation of the soft tissues, which can block the flow of air though the pharynx and vocal cords.
15

Central apnea occurs when there is a lack of respiratory effort. This may result from central nervous system immaturity, or from the effects of medications or illness. Many episodes of apnea of prematurity may start as either obstructive or central, but then involve elements of both, becoming mixed in nature.

SYMPTOMS Newborns, especially preemies, often have an irregular breathing pattern. These babies will have short episodes (5 - 10 seconds) of either shallow breathing or stopped breathing (apnea). These episodes are followed by periods of normal breathing. Bradycardia. Some babies may also have poor color and an ill-looking appearance. Apnea episodes that last longer than 20 seconds are considered serious.

16

TREATMENT How apnea is treated depends on the cause, how often the breathing stops, and the severity of spells. Babies who appear to be otherwise healthy and have few spells per day are simply watched. They can be gently stimulated during their occasional episodes. Babies who are well, but who have many episodes in which they stop breathing may be given a caffeine preparation to help stimulate their breathing. Sometimes the nurse will suction children with apnea, change their position, or use a bag and mask to help them breathe. Proper positioning, slower feeding time, oxygen, and (in extreme cases) a breathing machine may be needed to assist in breathing. Studies have not been able to show a benefit to putting babies on home monitors, so these monitors are no longer commonly used. Apnea of prematurity occurs in at least 85 percent of infants who are born at less than 34 weeks of gestation. The incidence is inversely related to the gestational maturity of the infant, but has considerable individual variability. Methylxanthines (theophylline and caffeine) have been used for almost three decades to treat apnea of prematurity.

17

Respiratory support

Simple tactile stimulation by touching the skin or patting the infant may stop an apneic episode by raising the infant's level of alertness. Increased oxygen at low levels can also be delivered using a nasal cannula, which additionally may provide some stimulation due to the tactile stimulation of the cannula. CPAP (continuous positive airway pressure) is sometimes used for apnea when medications and supplemental oxygen are not sufficient.

Mechanical ventilation is used to support infants whose apnea cannot be controlled sufficiently by other methods and where the potential risk of harm from recurrent hypoxia is felt to outweigh the risks of injury from ventilation.

In-hospital monitors in the NICU typically measure respiratory movements, heartrate, and pulse oximetry. Central apnea can be detected quickly since it results in absence of respiratory movements. Obstructive apnea can be detected when the level of oxygen has declined in the blood and/or results in slowing of the heart rate.

Home apnea monitors (which must be distinguished from infant monitors that are designed only to allow parents to listen to the infant remotely) most frequently measure only respiratory movements and/or heart rate. They are generally used with premature
18

infants who are otherwise ready for discharge, but who continue to require supplemental oxygen or medication for mild residual AOP. Home apnea monitoring is typically required for 612 weeks after discharge. PROGNOSIS Apnea of prematurity usually goes away by the baby's 36th week. Apnea is common in premature babies. Most babies have normal outcomes. Although mild apnea is not thought to have long-term effects, most doctors feel that preventing multiple or severe episodes is better for the baby over the long-term. Apnea episodes that began after the second week of life or that last longer than 20 seconds are considered more serious. PERINATAL ASPHYXIA INTRODUCTION Birth asphyxia occurs when a baby does not receive enough oxygen before, during or just after birth. It occurs during the first and second stage of labor and is identified by fetal acidosis, as measured in umbilical arterial blood. Hypoxic damage can occur to most of the infant's organs (heart, lungs, liver, gut, kidneys), but brain damage is of most concern and perhaps the least likely to quickly or completely heal. Birth asphyxia is also called asphyxia neonatorum or newborn asphyxia. DEFINITION Birth asphyxia is defined as failure to initiate and maintain spontaneous respiration following birth and is characterized by hypoventilation, anaerobic glycolysis and lactic acidosis. Birth asphyxia is defined as failure of efficient pulmonary respiration at birth with hypoxia and acidemia. It is the medical condition resulting from deprivation of oxygen to a newborn infant that lasts long enough during the birth process to cause physical harm, usually to the brain. ESSENTIAL CRITERIA FOR ASPHYXIA

19

Prolonged metabolic or mixed academia ( pH less than 7 ) on an umbilical arterial blood sample. Persistence of apgar score of 0-3 for more than 5 minutes. Neurological manifestations: seizure, coma, hypotonia, hypoxic ischemic encephalopathy (HIE) in the immediate neonatal period. Evidence of multi organ dysfunction in the immediate neonatal period. American Academy of Pediatrics.

INCIDENCE Perinatal asphyxia happens in 2 to 10 per 1000 newborns that are born at term, and more for those that are born prematurely. CAUSES In term infants 90% of asphyxial events occur in the ante partum or intrapartum period, as a result of impaired gas exchange across the placenta that leads to the inadequate provision of oxygen and removal of carbon dioxide and H+ from the fetus. Failure of respiratory center by prolonged hypoxia, trauma, maternal sedatives and immaturity. Failure of pulmonary expansion (atelectasis) due to low alveolar surfactant and poor respiratory movements of preterm baby. Impairment of maternal oxygenation. Decreased blood flow from mother to placenta. Decreased blood flow from placenta to fetus. Impaired gas exchange across the placenta or at the fetal tissue level. Increased fetal oxygen requirement. thick meconium stained amniotic fluid

Factors that may lower oxygen in the baby after birth include: Severe anemia or a low blood cell count Low blood pressure or shock.
20

Heart or lung disease.

Other factors include: Maternal factors such as hypertension, infection, diabetes, hypotension, drug use, other systemic disorders. Placental factors: infarction, fibrosis, abruption or hydrops. Uterine rupture. Umbilical cord accidents: true knot, compression. Fetal factors: anemia, infection, Neonatal factors: cyanotic congenital heart disease, persistent pulmonary hypertension of newborn. Study conducted in Department of Pediatrics, Siriaj Hospital, Thailand concluded that abnormal fetal heart rate pattern, thick meconium stained amniotic fluid, and premature delivery, were three common risk factors for asphyxia. CLINICAL FEATURES The clinical features depend upon the etiology, intensity and duration of oxygen lack, plasma carbon dioxide excess and subsequent acidosis. According to the intensity of clinical features, they have been classified previously as asphyxia livida (stage of cyanosis) and asphyxia pallida (stage of shock). But at present, according to the parameters denoted by Apgar, the apgar scoring system is used widely. Clinical sequences of birth asphyxia: Initial response is hyperpnoea and hypertension Breath blood flow secondary apnea cerebral hemorrhage primary apnea gasping attempt to diminished cerebral (if severe)

bradycardia and shock

hypoxic ischemic encephalopathy

either death or handicap.

21

The symptoms of asphyxia neonatorum are bluish or gray skin color (cyanosis), slow heartbeat (bradycardia), stiff or limp limbs (hypotonia), and a poor response to stimulation, gasping or weak breathing, meconium stained liquor amnii. MULTI ORGAN DYSFUNCTION IN PERINATAL ASPHYXIA CNS Pulmonary Renal Metabolic : HIE, cerebral edema, seizures. : pulmonary hypertension, meconium aspiration, surfactant disruption. : oliguria, acute renal failure. : metabolic acidosis, hypoglycemia, hypocalcemia.

Gastro intestinal: NEC, hepatic dysfunction. Hematological : DIC. Neurological: HIE: The main cause of HIE is fetal asphyxia. Recognition of neonatal hypoxic ischemic encephalopathy (HIE) re- quires careful observation and examination as the spectrum of signs which may be found in HIE , varies with the severity of the insult. With prolonged asphyxia, cerebral blood flow becomes dependent on systemic BP. A decrease in CO causes hypotension and impaired cerebral blood flow resulting in anaerobic metabolism and eventual intracellular energy failure due to an increase in the utilization of glucose in the brain and a fall in the concentration of glycogen, phosphocreatine and ATP. Signs are mainly characterized by abnormalities of tone, altered consciousness, and seizures which may occur in up to 70% of infants with moderate to severe HIE by the end of the first day of life. Potential benefit of preventing further neonatal injury associated with seizures following asphyxia has promoted the widespread use of anticonvulsants, barbiturates in particular, for the prevention of seizures. The main features of HIE include the following:

22

Apgar score less than 3 for more than 5 minutes. Fetal heart rate less than 60 beats /minute. Prolonged antenatal acidosis. Seizure within first 24-48 hours after birth. Burst suppression pattern EEG.

Sarnat and Sarnat Stages of Hypoxic Ischemic Encephalopathy STAGE LOC Neuromuscular control Muscle tone Posture Stretch reflexes Segmental myoclonus Complex reflexes suck moro Oculovestibular Tonic neck Pupils STAGE 1(MILD) hyper alert; irritable Uninhibited, over reactive normal Mild distal flexion Over active Present/absent normal weak Strong, low threshold normal Slight Mydriasis STAGE 2 (MOD) Lethargic, obtunded Diminished spontaneous movement Mild hypotonia Strong distal flexion Over active, disinhibited present suppressed Weak/ absent Incomplete, high threshold overactive strong Miosis STAGE 3 (SEVERE) Stuporous, comatose Diminished or absent spontaneous movement flaccid Intermittent decerebration Decreased or absent absent absent absent absent absent absent Midposition, often unequal, poor light reflex Periodic; apnoea. Variable. Variable. Variable.

Respiration Heart rate

Spontaneous Tachycardia

Occasional apnoea Bradycardia Profuse Increased diarrhea

Bronchial and salivary Sparse secretions GI motility Normal/decreased

23

Seizures

None

Common focal/ multifocal 2-14 days 80% normal; abnormal if more than 5-7 days.

Duration of symptoms Less than 24 hours Outcome About 100 normal

Uncommon (excluding decerebration) Hours to weeks. About 50% die; remainder with severe sequel.

SEIZURES Described in 20% to 50% of infants with HIE, and usually starts between 6 and 24 hours after the insult. CEREBRAL PALSY Premature babies delivers decreased oxygen to the brain and this causes cerebral palsy. Blood clots in the brain also causes this. Renal Proximal tubule of the kidney is especially affected by decreased perfusion, leading to acute tubular necrosis. It is recognized by a rising plasma creatinine concentration, or by oliguria, defined as an hourly urine flow of less than 0.5 ml/kg. Clinical management, however, is more often determined by the urine flow rate and a useful test is to observe the response to frusemide 1-5 mg/kg, given following a fluid challenge (10-20 ml/kg). In the case of a poor response there is no value in repeating the challenge as frusemide is excreted renally and will remain in the circulation for some time, and many babies with acute renal failure develop fluid overload. GI effects Increased risk of bowel ischemia and NEC. Cardiovascular

A common accompaniment to birth asphyxia is myocardial ischemia leading to cardiac dysfunction and systemic hypo- tension. This leads to under-perfusion of peripheral tissues and vital organ systems, i.e., 'shock', thus causing the already compromised brain to be further under-perfused. Clinical signs of cardiac dysfunction and peripheral systemic under
24

perfusion include delayed capillary refill, bradyarrhythmias and increased core-peripheral temperature gradient. Hypotension is a late sign of under- perfusion. The cause of hypotension is rarely blood loss and is more often due to peripheral vaso-dilatation or poor cardiac output. If available, echocardiography provides a useful assessment of cardiac function. In our practice, even if the infant is normotensive, we routinely obtain a chest X-ray to check for cardiomegaly and an echocardiogram to check for evidence of cardiac dysfunction. Hematologic effects Damage to blood vessels Poor production of clotting factors due to liver dysfunction Poor production of platelets by bone marrow This is a well recognized complication of birth asphyxia and requires prompt treatment with platelets, fresh frozen plasma and cryo precipitate Pulmonary effects Increased pulmonary vascular resistance, pulmonary edema due to cardiac dysfunction, secondary RDS due to failure of surfactant production, and meconium aspiration. DIAGNOSIS Perinatal assessment of risk includes awareness of pre existing maternal or fetal problems that may predispose to perinatal asphyxia. Diagnosis can be objectively assessed using the Apgar score a recording of the physical health of a newborn infant, determined after examination of the adequacy of respiration, heart action, muscle tone, skin color, and reflexes. Normally, the Apgar score is of 7 to 10. Infants with a score between 4 and 6 have moderate depression of their vital signs while infants with a score of 0 to 3 have severely depressed vital signs and are at great risk of dying unless actively resuscitated. Severe acid levels: pH less than 7 in the arterial blood of the umbilical cord. Neurological problems such as seizure, coma and poor muscle tone.
25

DIC.

Day to day baseline investigations should include serum electrolytes, liver and renal function tests, coagulation studies and arterial blood gases. Because of multisystem involvement in babies with severe birth asphyxia, it only helps to seek advice from other specialist colleagues.

MANAGEMENT Management of perinatal asphyxia can be divided into two: prophylactic and definitive. Prophylactic: Antenatal detection of high risk cases. Regular fetal monitoring- monitoring of fetal distress (both antenatal and intranatal) and timely delivery is essential. giving the mother extra amounts of oxygen before delivery. Scalp blood pH assessment: scalp blood pH <7.0 is a substantial evidence of prolonged intrauterine asphyxia. It is a vaginal procedure, when women is in active labor. It takes nearly 5 minutes. Women will be in lithotomy position, cervix 3-4 cm dilated. Plastic cone is placed in the vagina against fetal scalp and scalp is pierced. This help to determine the wellbeing of the baby. Definitive: APGAR SCORING at 1 minute and 5 minute after birth. CRITERIA Respiration Heat rate Muscle tone Reflex response Skin color 0 Absent Absent Flaccid No response Blue, pale 1 Slow, irregular Slow(below 100) Some flexion of extremities Grimace Body pink, extremities blue 2 Good, crying More than 100 Active body movements cry Completely pink

Total score = 10 No depression : 7-10

26

Mild depression : 4-6 Severe depression :0-3 The normal routine procedure is to be followed as soon as the baby is born. Hold the

baby by legs with head down. Suck the mouth & the pharynx, with a catheter attached to a mucus sucker or a suction apparatus, if available. At this point most babies will gasp & cry, the breathing will be established.

Mildly asphyxiated Clamp the cord and separate the baby. Wipe the baby Wrap in dry, warm towel. Place under preheated area or radiant warmer. Oropharynx and nasopharynx are to be cleared off any mucus by suction. Oxygen if required. The condition is reassessed at 5 minute. Babies feet are patted, back is rubbed, the baby cries.

Moderately depressed apgar score ( 4-6) Positive pressure ventilation by ambu bag. Extend the babys neck. Majority starts respiration and cries.

Severely depressed baby (apgar score upto 3) The treatment is resuscitation of the newborn. If stimulation fails to initiate regular respiration in the newborn, the attending physician attempts resuscitation. Most term asphyxiated infants, if adequately ventilated, even in room air, will recover. High concentrations of supplemental oxygen. (80%-100%) are usually recommended. Presence of thick meconium stained liquor at the time of delivery presents a special situation. Isotonic saline is as effective as 5% albumin for treating hypotension or as volume re- placement, and has the additional advantage of causing less fluid retention in the first 48 hours.

27

The 2010 guidelines on neonatal resuscitation In 2010, the American Heart Association (AHA), the European Resuscitation Council (ERC) and the International Liaison Committee on Resuscitation (ILCOR) issued new guidelines on newborn resuscitation.

28

29

WEIGHT OF THE NEWBORN 1 KG 2 KG 3KG.

ETT DEPTH 7 CM 8 CM 9 CM

APPROPRITAE ET DEPTH= WT +6 UPTO 3 KG.

APPROPRITE ETT DEPTH FOR MORE THAN ONE YEAR= AGE IN YEARS +12 2

MILLERBLADES.

LARYNGEAL MASK AIRWAY

30

Advantages of LMA; No need of laryngoscopy Less trauma to local tissues and respiratory tract.

Treatment may also include the following:

extracorporeal membrane oxygenation (ECMO) ECMO is a technique similar to a heart-lung bypass machine, which assists the infant's

heart and lung functions with use of an external pump and oxygenator. It delivers oxygen to the babys brain and body as temporary support. Blood is shunted from a catheter in the right atrium or right internal jugular vein by gravity to a servo regulated roller pump, pumped through a membrane lung where it is oxygenated, through a small heat exchanger where it is warmed, and then return to the systemic circulation through a major artery such as the carotid artery to the aortic arch.

31

The results of study conducted by Department of Pathology, Johns Hopkins Hospital, Baltimore, MD 1993 July, shows that qualitative and quantitative platelet changes occur while a neonate is receiving ECMO. The survival rate of transfused platelets is reduced, and the acquired platelet dysfunction is not reversed by the transfusion of platelets with normal function while the patient is receiving ECMO. Surfactant therapy

Respiratory epithelial cells are of 2 types: type 1 cells and type 2 cells. Type 2 cells contain osmiophiic lamellar bodies that contain surfactant. Surfactant is made of 84% phospholipids, 8% neutral lipids and 8% proteins. This reduces the surface tension. After 35th week, mature level of surfactant will be produced. Premature infants do not have adequate amount of surfactant to survive extrauterine life. Surfactant is mainly extracted from bovine, porcine or calf lung extract and is given through endotracheal tube.
Further Management

Even when the infant is not in need of artificial ventilation following resuscitation, babies who have required intensive resuscitation are often brought to the intensive care unit for further monitoring and close follow up for evidence of any systemic impairment.

seizures: Treatment of seizures can often be difficult and may require multiple anticonvulsant therapy.

Phenobarbitone: This is used as a first line anticonvulsant for the control of neonatal seizures, given as an initial loading dose of 20 mg/kg IV in order to ensure optimal therapeutic serum concentration. If adequate Control is not achieved, a further dose, 5mg/kg should be repeated within half an hour up to a total dose of 40 mg/k or control of seizures. Fosphenytoin: Given in a loading dose of 20 mg/kg IV over at least 20 minutes, if phenobarbitone fails to control seizures. If not persist, additional dose of 5mg/kg can be given.

Other anticonvulsants include lorazepam, diazepam, midazolam etc.

32

 Tubular necrosis: In most cases, renal failure resulting from acute tubular necrosis improves with conservative treatment which includes strict management of fluid and electrolyte balance. This requires meticulous calculation of fluid input and output at 12 hourly intervals. Urinary retention is a common occurrence in asphyxiated babies, and such babies need to be catheterized in order to obtain an accurate measure of output. To this any insensible loss of 30-40 ml/kg/day, and any other losses such as gastrointestinal losses are added. Total fluid output should be replaced exactly, ml for ml. Although this can be done using a single intravenous fluid, we prefer to establish two peripheral intravenous lines allowing infusion rates to be titrated against losses. We replace insensible loss with 20% glucose (without sodium). The second infusion can be used to replace other measured fluid losses volume for volume using a fluid type dependent upon the fluid lost. It is essential to measure and not to guess the electrolyte concentrations of the losses. If there is evidence of global ventricular dysfunction, we start treatment with a combination of dopamine and dobutamine in low doses (each up to 5 mcglkg/minute), titrated if necessary against the response (up to 10-15 mcg/kg/minute). Dopamine is a more effective agent if an increase in systemic blood pressure is required; however, if cardiac output is poor, dopamine will cause a reduction in tissue perfusion. Dobutamine is used in order to bring about an increase in cardiac output. Both dopamine and dobutamine are inactivated by bicarbonate or any alkaline solution, and hence should not be infused through the same line. Epinephrine has been used in cases of post-asphyxial cardiac failure refractory to other inotropes (0.1 mcg/kgl minute-up to a maximum of 1.5 mcg/kgl minute) but it is increasingly felt that such a requirement identifies individual babies as profoundly asphyxiated and raises the question of the appropriateness of continuing treatment. Exuberant use of volume expansion may be detrimental and should be discouraged unless there is evidence of volume depletion. Monitoring of central venous pressure (CVP) would be ideal in such cases but it's routine use is hampered by technical difficulties in the newborn population. As there is no other measurement of right ventricular preload, central venous pressure (CVP) measurement pro- vides important hemodynamic information. CVP is not measured routinely in neonatology and there is shortage of data. Values over 7-8 mmHg are found in babies with myocardial dysfunction or circulatory failure.

33

PROGNOSIS The prognosis for asphyxia neonatorum depends on how long the new born is unable to breathe. For example, clinical studies show that the outcome of babies with low five-minute Apgar scores is significantly better than those with the same scores at 10 minutes. With prolonged asphyxia, brain, heart, kidney, and lung damage can result and also death, if the asphyxiation lasts longer than 10 minutes. PREVENTION Anticipation is the key to preventing asphyxia neonatorum. It is important to identify fetuses that are likely to be at risk of asphyxia and to closely monitor such high-risk pregnancies. High-risk mothers should always give birth in hospitals with neonatal intensive care units where appropriate facilities are available to treat asphyxia neonatorum. During labor, the medical team must be ready to intervene appropriately and to be adequately prepared for resuscitation. PARENTAL CONCERNS Women at risk for asphyxia neonatorum pregnancies should receive focused prenatal care from an obstetrician skilled at preventing and detecting problems such as anemia that may contribute to asphyxia neonatorum. While prenatal care will not necessarily prevent newborn asphyxia, it can help ensure that both the mother and her baby are as healthy as possible at the time of birth. CONCLUSION Perinatal asphyxia contributes greatly to neonatal mortality and morbidity. In developing countries, the need for risk assessment in perinatal asphyxia is obvious because of the high birth rate and limited perinatal resources. Immediate and essential care of the new born is very essential in reducing mortality.

34

MECONIUM ASPIRATION SYNDROME Acute or chronic hypoxia and/or infection can result in the passage of meconium in utero. In this setting, gasping by the fetus or newly born infant can cause aspiration of amniotic fluid contaminated by meconium. Meconium aspiration before or during birth can obstruct airways, interfere with gas exchange, and severe respiratory distress. INCIDENCE Meconium stained amniotic fluid (MSAF) complicates delivery in approximately 8% to 15% of live births. The incidence of MSAF in preterm infants is very low. Most babies with MSAF are 37 weeks or older, and most meconium stained infants are post mature and small for gestational age. PATHOPHYSIOLOGY Meconium is a sterile, thick, black green odorless material that results from the accumulation of debris is the fetal intestine during the third month of gestation. The components of meconium include: water (72%-80%), desquamated cells from the intestine and skin, gastro intestinal mucin, lanugo hair, fatty material from the vernix caseosa, amniotic fluid and intestinal secretions, blood-group specific glycoproteins and biles. Passage of meconium in utero: MSAF may result from a post-term fetus with rising motilin levels and normal gastrointestinal function, vagal stimulation produced by cord or head compression, or in utero fetal distress. Amniotic fluid that is thinly stained is described as watery. Moderately stained fluid is opaque without particles and fluid with thick meconium with particles is sometimes called pea soup. Aspiration of meconium: In the presence of fetal distress, gasping by the fetus can result in aspiration of meconium before, during or immediately following delivery. Severe MAS appears to be caused by pathologic intrauterine processes, primarily chronic hypoxia, acidosis and infection. Meconium has been found in the lungs of stillborn infants and infants who died soon after birth without a history of aspiration at delivery.
35

Effects of meconium aspiration:

When aspirated into the lung, meconium may stimulate the release of cytokines and vasoactive substances that result in cardiovascular and inflammatory responses in the fetus and newborn. Meconium itself, or the resultant chemical pneumonitis, mechanically obstructs the small airways, causes atelactasis and a ballvalve effect with resultant air trapping and possible air leak. Aspirated meconium leads to vasospasm, hypertrophy of the pulmonary arterial musculature, and pulmonary hypertension that leads to extra pulmonary right to left shunting, through the ductus arteriosus or the foramen ovale and results in worsened ventilation-perfusion mismatch, leading to severe arterial hypoxemia. Approximately one third of infants with MAS develop persistent pulmonary hypertension of the new born (PPHN), which contributes to the mortality associated with this syndrome. Aspirated meconium also inhibits surfactant function. CLASSIFICATION OF MAS: Mild MAS requires less than 40% oxygen for less than 48 hours. Moderate MAS requires more than 40% oxygen for more than 48 hours without air leak. Severe MAS requires assisted ventilation for more than 48 hours, often associated with PPHN.

36

PATHOPHYSIOLOGY Meconium aspiration

Mechanical obstruction

clinical inflammation

surfactant inactivation

incomplete

complete

atelectasis

Ball value obstruction

intra pulmonary shunting

Atelectasis.

Hypoxia Acidosis

PREVENTION OF MAS Prevention of passage of meconium in utero

Mothers at risk for uteroplacental insufficiency include those with preeclampsia or increased BP, chronic respiratory or cardio vascular disease, poor uterine growth, post-term pregnancy, and heavy smokers.these women should be carefully monitored during pregnancy. Monitor FHR during labor. Obtain fetal scalp blood for PH. Amnioinfusion.
37

This treats repetitive variable fetal heart rate decelerations by relieving umbilical cord compressions in labor. Timing and mode of delivery

In pregnancies that continue past the due date, induction as early as 41 weeks may help prevent MAS by avoiding passage of meconium. Delivery mode does not appear to significantly impact the risk of aspiration. MANAGEMENT OF INFANTS DELIVERED THROUGH MECONIUM-STAINED FLIUD. a. Initial assessment See whether the baby demonstrates heart rate more than 100 / minute, spontaneous respiration and good tone. b. Suctioning technique Infant should be placed on radiant warmer and given free-flow oxygen. Delay drying and stimulation, and postpone emptying of any gastric contents until the infant has stabilized. Intubate, preferably before respiratory efforts have been initiated. After intubation, the tube is attached to wall suction at a pressure of 80-100 mm Hg by means of a plastic adapter. Continuous suction is applied as the tube is being withdrawn; the procedure is repeated until the trachea is cleared or resuscitation needs to be initiated. Avoid positive pressure ventilation, if possible, until tracheal suctioning is accomplished. MANAGEMENT OF MAS A. Observation: Observe for the features of respiratory distress. Monitor oxygen saturation. Chest radiograph is helpful in determining this. The classic findings are diffuse, asymmetric patchy infiltrates, areas of consolidation and hyperinflation. B. Routine Care Baby should be maintained in a neutral thermal environment and tactile stimulation should be minimized.
38

Assess blood glucose and calcium levels. Severely depressed babys may have severe metabolic acidosis and it need to be corrected. Fluids should be restricted as much as possible to prevent cerebral and pulmonary edema. Monitor for hypotension and poor cardiac output. Circulatory support with normal saline or packed red blood cells should be provided in patients with marginal oxygen. Renal function should be continuously monitored.

C. Oxygen Therapy Management of hypoxemia should be accomplished by increasing the inspired oxygen concentration and by monitoring blood gases and PH. An indwelling arterial catheter is usually required for blood sampling. It is crucial to provide sufficient oxygen, because repeated hypoxic insults may result in ongoing pulmonary vasoconstriction and contribute to the development of PPHN. D. Assisted ventilation Continuous positive airway pressure Mechanical ventilation. It is indicated for excessive carbon dioxide retention (Pa co2 > 60 mm Hg) or for persistent hypoxemia (Pa o2 < 50 mm Hg).
-

In these infants, higher inspiratory pressures (approximately 30-35 cm H2O) are more often required than in infants with RDS; the PEEP selected (usually 3-6 cm H2 O) depends on the individuals response. Adequate expiratory time should be permitted to prevent air trapping behind partly obstructed airways.

High-frequency ventilation with jet or oscillatory ventilators may be successful in infants with severe MAS who fail to improve with conventional ventilation, and in those who develop air-leak syndromes.

E. Medications Antibiotics: broad spectrum antibiotic (eg: ampicillin and gentamycin) is usually indicated in infants when an infiltrate is seen on chest radiograph. Blood cultures should be obtained to identify bacterial disease. Surfactant:

39

Endogenous surfactant activity may be inhibited by meconium. Surfactant treatment of MAS may improve oxygenation and reduce pulmonary complications and the need for extracorporeal membrane oxygenation (ECMO).

Corticosteroids: This reduce inflammation induced by meconium and minimize prostaglandin mediated pulmonary vasoconstriction.

COMPLICATIONS Air Leak: Pneumothorax or pneumo mediastinum occurs in approximately 15%-33% of patients with MAS. Air leaks occur more frequently with mechanical ventilation. PPHN: It is associated with MAS in approximately one third of cases and contributes to the mortality associated with this syndrome. In severely ill infants with MAS and PPHN, inhaled nitric oxide reduces the need for ECMO. Pulmonary sequele: Approximately 5% of survivors require supplemental oxygen at 1 month, and a substantial proportion may have abnormal pulmonary function, including increased functional residual capacity, airway reactivity and higher incidence of pneumonia.

RESPIRATORY DISTRESS SYNDROME Neonatal respiratory distress syndrome (RDS) is most commonly a complication seen in premature infants. The condition makes it difficult to breathe. It is due to developmental delay in lung maturation. Without treatment, the infant will die within a few days after birth, but if oxygen can be provided, and the infant receives modern treatment in a neonatal intensive care unit, complete recovery with no after-effects can be expected. DEFINITION Respiratory distress syndrome (RDS) of the newborn, previously known as Hyaline Membrane Disease (HMD), is an acute lung disease present at birth, which usually affects
40

premature babies and is characterized by respiratory rate more than 60 br/mt, expiratory grunting, cyanosis and vicious cycle of hypoxia.

RISK FACTORS AND CAUSES

Prematurity- most cases are seen in babies born before 28 weeks. The disease is mainly caused by a lack of a slippery, protective substance called surfactant, which helps the lungs inflate with air and keeps the air sacs from collapsing. It can also be the result of genetic problems with lung development.

In addition to prematurity, the following increase the risk of neonatal RDS:

Perinatal asphyxia Diabetes in the mother Cesarean delivery cardiac disorders Meconium aspiration syndrome TEF Delivery complications that lead to acidosis in the newborn at birth Multiple pregnancy (twins or more) Rapid labor
41

Chorioamnionitis drugs

The risk of neontal RDS may be decreased if the pregnant mother has chronic, pregnancy-related high blood pressure or prolonged rupture of membranes, because the stress of these situations cause the infant's lungs to mature sooner. PATHOPHYSIOLOGY Due to various etiological factors Damage to type 2 alveolar cells occurs Decreased surfactant Alveolar atelectasis, hypoventilation Decreased Pa02 and decreased pH. SCORING SYTEM FOR RDS Downes score: Sign
Respiratory rate Cyanosis Grunt Retractions Air entry on crying

0
Less than 60 None None None Good

1
60-80 In room air Audible with stethoscope Mild Decreased

2
More than 80 Even In 40% oxygen Audible without stethoscope Moderate Barely audible.

SYMPTOMS The symptoms usually appear within minutes of birth, although they may not be seen for several hours. Respiratory signs and symptoms may include:

Tachypnoea Dyspnoea
42

Pronounced intercostas and or substernal retractions Fine inspiratory crackles Audible expiratory grunt Flaring of the external nares Cyanosis or pallor

Manifestations as the disease progresses:

Apnea Flaccidity Absent spontaneous movement Unresponsiveness Diminished breath sounds Mottling

Manifestations associated with severe disease

Shock like state Decreased cardiac output and bradycardia Low systemic BP.

DIAGNOSTIC EVALUATION Diagnosis is made on the basis of clinical manifestations. A blood gas analysis shows low oxygen and excess acid in the body fluids. On radiography, diffuse granular pattern over both lung fields that closely resembles . "ground glass" appearance, which often develops 6 to 12 hours after birth. Dark streaks, or bronchograms, within the ground glass area that represent dilated, airfilled bronchioles. Lung function studies may be needed. Lab tests are done to rule out infection and sepsis as a cause of the respiratory distress.

MANAGEMENT High-risk and premature infants require prompt attention by a neonatal resuscitation team.
43

 Immediate establishment of adequate oxygenation and ventilation. Infants will be given warm, moist oxygen. This is critically important, but needs to be given carefully to reduce the side effects associated with too much oxygen. Maintain acid base balance. Maintain a neutral thermal environment Maintain adequate tissue perfusion and oxygenation. Prevent hypotension Maintain adequate hydration and electrolyte status. Nipple and gavage feedings are contraindicated in any situation that creates a marked increase in respiratory rate because of the hazard of aspiration. CPAP: A treatment called continuous positive airway pressure (CPAP) that delivers slightly pressurized air through the nose can help keep the airways open and may prevent the need for a breathing machine for many babies. Even with CPAP, oxygen and pressure will be reduced as soon as possible to prevent side effects associated with excessive oxygen or pressure. A variety of other treatments may be used, including:

Extracorporeal membrane oxygenation (ECMO) to directly put oxygen in the blood if a breathing machine can't be used.

Inhaled nitric oxide to improve oxygen levels Surfactant Replacement therapy in Neonatal Respiratory Distress Syndrome (NRDS)

44

Composition of pulmonary surfactant:

40% dipalmitoylphosphatidylcholine (DPPC) 40% other phospholipids (PC) 5% surfactant-associated proteins (SP-A, B, C and D) Cholesterol (neutral lipids) Traces of other substances.

Complications of surfactant therapy: plugging of endotracheal tube (ETT) by surfactant desaturation and increased need for supplemental O2 bradycardia due to hypoxia tachycardia due to agitation, with reflux of surfactant into the ETT pharyngeal deposition of surfactant; administration of surfactant to only one lung; administration of suboptimal dose secondary to miscalculation or error in reconstitution. Physiologic complications of surfactant replacement therapy include: apnea, pulmonary hemorrhage, mucus plugs, increased necessity for treatment for PDA, marginal increase in retinopathy of prematurity, barotrauma resulting from increase in lung compliance following surfactant replacement and failure to change ventilator settings accordingly. It is important that all babies with RDS receive excellent supportive care, including the following, which help reduce the infant's oxygen needs:

45

Few disturbances Gentle handling Maintaining ideal body temperature

PROGNOSIS The condition often worsens for 2 to 4 days after birth with slow improvement thereafter. Some infants with severe respiratory distress syndrome will die, although this is rare on the first day of life. If it occurs, it usually happens between days 2 and 7.Long-term complications may develop as a result of oxygen toxicity, high pressures delivered to the lungs, the severity of the condition itself, or periods when the brain or other organs did not receive enough oxygen. PREVENTION Preventing prematurity is the most important way to prevent neonatal RDS. Ideally, this effort begins with the first prenatal visit, which should be scheduled as soon as a mother discovers that she is pregnant. Good prenatal care results in larger, healthier babies and fewer premature births. Avoiding unnecessary or poorly timed cesarean sections can also reduce the risk of RDS. Assess the maturity of the lungs by amniocentesis. In some cases, medicines called corticosteroids may be given to help speed up lung maturity in the developing baby. They are often given to pregnant women between 24 and 34 weeks of pregnancy who seem likely to delivery in the next week. The therapy can reduce the rate and severity of RDS, as well as the rate of other complications of prematurity, such as intraventricular hemorrhage, patent ductus arteriosus, and necrotizing enterocolitis. It is not clear if additional doses of corticosteroids are safe or effective. NURSING DIAGNOSIS Ineffective breathing pattern related to surfactant deficiency, alveolar instability, and pulmonary immaturity. Impaired gas exchange related to immature alveolar structure. Impaired gas exchange related to inability to maintain lung expansion.
46

BRONCHOPULMONARY DYSPLASIA
Bronchopulmonary dysplasia (BPD) is a chronic lung condition that affects newborn babies who were either put on a breathing machine after birth or were born very early (prematurely). CAUSES Bronchopulmonary dysplasia (BPD) occurs in severely ill infants who have received high levels of oxygen for long periods of time or who have been on a breathing machine (ventilator). It is more common in infants born early (prematurely), whose lungs were not fully developed at birth. Risk factors include:

Congenital heart disease Prematurity, usually in infants born before 32 weeks gestation Severe respiratory or lung infection

SYMPTOMS

Bluish skin color (cyanosis) Cough Rapid breathing Shortness of breath

DIAGNOSTIC MEASURES

Arterial blood gas Chest CT scan Chest x-ray Pulse oximetry

TREATMENT IN THE HOSPITAL:

47

A breathing machine (ventilator) is usually needed to send pressure to the lungs to keep the baby's lung tissue inflated, and to deliver more oxygen. Pressures and oxygen levels are slowly reduced. After being weaned from the ventilator, the infant may continue to get oxygen by a mask or nasal tube for several weeks or months.

Infants with BPD are usually fed by tubes inserted into the stomach (NG tube). These babies need extra calories due to the effort of breathing. Infants may need to limit fluids, and may be given medications that remove water from the body (diuretics) to keep the lungs from filling with fluid. Other medications can include corticosteroids, bronchodilators, and surfactant.

Parents of these infants need emotional support, because it can take time for the disease to get better, and the infant may need to stay in the hospital for a long time. AT HOME: Infants with BPD may need oxygen therapy for weeks to months after leaving the hospital. It is very important for all infants with chronic lung disease to receive enough calories as they recover. Many will need tube feedings or special formulas.

Care to be taken to prevent RSV.A simple way to help prevent RSV infection is to wash your hands often, especially before touching your baby. Insist that others wash their hands with warm water and soap before touching the baby.

Have others avoid contact with your baby if they have a cold or fever. If necessary, it may be helpful for them to wear a mask.

Be aware that kissing your baby can spread RSV infection. Try to keep young children away from your baby. RSV is very common among young children and easily spreads from child to child.

Exposure to tobacco smoke increases the risk of RSV illness. Avoid crowds during outbreaks of RSV. Moderate-to-large outbreaks are often reported in the local news and newspapers to provide parents with an opportunity to avoid exposure.

PROGNOSIS

48

Babies with BPD get better slowly over time. It's possible for infants to need oxygen therapy for many months. Some infants with this condition might not survive. Some children are left with long-term lung damage. POSSIBLE COMPLICATIONS Babies who have had BPD are at greater risk for repeated respiratory infections, such as pneumonia, bronchiolitis, and respiratory syncytial virus (RSV) that require a hospital stay. Other potential complications in babies who have had BPD are:

Developmental problems Poor growth Pulmonary hypertension

OTHER DISORDERS OF HIGH RISK NEWBORN

RETINOPATHY OF PREMATURITY

Retinopathy of prematurity (ROP), previously known as retrolental fibroplasia (RLF), is an eye disease that affects prematurely-born babies. It is thought to be caused by disorganized growth of retinal blood vessels which may result in scarring and retinal detachment. ROP can be mild and may resolve spontaneously, but it may lead to blindness in serious cases. Both oxygen toxicity and relative hypoxia can contribute to the development of ROP. RISK FACTORS low gestational age Low birth weight. Prolonged oxygen exposure

49

POSSIBLE MECHANISMS OF INJURY It consists of 2 stages. In the first stage, it involves an initial insult such as hyperoxia, hypoxia or hypotension at a critical point in retinal vascularization that results in vasoconstriction and decreased blood flow to the retina with a subsequent arrest in vascular development. In the second stage, neovascularization occurs. New vessels grow through the retina into the vitreous. These vessels are permeable and hemorrhage and edema can occur. Extensive and severe extraretinal fibrovascular proliferation can lead to retinal detachment and abnormal retinal function. DIAGNOSIS Following pupillary dilation using eye drops, the retina is examined using a special lighted instrument (an indirect ophthalmoscope). The peripheral portions of the retina are sometimes pushed into view using scleral depression. Retinal examination with scleral depression is generally recommended for patients born before 3032 weeks gestation, with birthweight 1500 grams or less, or at the discretion of the treating neonatologist. The initial examination is usually performed at 46 weeks of life, and then repeated every 13 weeks until vascularization is complete (or until disease progression mandates treatment). INTERNATIONAL CLASSIFICATION OF RETINOPATHY OF PREMATURITY (ICROP) The system used for describing the findings of active ROP is entitled The International Classification of Retinopathy of Prematurity (ICROP). ICROP uses a number of parameters to describe the disease. They are location of the disease into zones (1, 2, and 3), the circumferential extent of the disease based on the clock hours (1-12). The circumferential extent of the disease is characterized by

Stage 1 is a faint demarcation line. Stage 2 is an elevated ridge.

50

Stage 3 is extraretinal fibrovascular tissue. Stage 4 is sub-total retinal detachment. Stage 5 is total retinal detachment.

PROGNOSIS Stages 1 and 2 do not lead to blindness. However, they can progress to the more severe stages. Progression to stage 4 (partial retinal detachment), or to stage 5 (total retinal detachment), will result in substantial or total loss of vision for the infant. TREATMENT The silicone band (scleral buckle, blue) is placed around the eye. This brings the wall of the eye into contact with the detached retina, allowing the retina to re-attach.

Scleral buckling and/or vitrectomy surgery may be considered for severe ROP (stage 4 and 5) for eyes that progress to retinal detachment.

Intravitreal injection of bevacizumab (Avastin) has been reported as a supportive measure in aggressive posterior retinopathy of prematurity.

The retina (red) is detached at the top of the eye.

51

NEONATAL HYPERBILIRUBINEMIA DEFINITION Neonatal jaundice or Neonatal hyperbilirubinemia is a yellowing of the skin and other tissues of a newborn infant. A bilirubin level of more than 85 umol/l (5 mg/dL) manifests clinical jaundice in neonates whereas in adults a level of 34 umol/l (2 mg/dL) would look icteric. In neonates the dermal icterus is first noted in the face and as the bilirubin level rises proceeds caudal to the trunk and then to the extremities. In newborns jaundice is detected by blanching the skin with digital pressure so that it reveals underlying skin and subcutaneous tissue. Jaundice newborns have an apparent icteric sclera, and yellowing of the face, extending down onto the chest. BILIRUBIN Non-polar, water insoluble compound requiring conjugation with glucuronic acid to form a water soluble product that can be excreted. It circulates to the liver reversibly bound to albumin Bilirubin physiology Increased production in neonate due to larger red cell volume, which produces bilirubin as cells are broken down and shorter RBC life span, so broken down faster. Heme is catabolized within the reticuloendothelial system by heme oxygenase to form biliverdin. Biliverdin is metabolized to bilirubin in the presence of biliverdin reductase Ligandins responsible for transport from plasma membrane to endoplasmic reticulum. Bilirubin conjugated in presence of UDPGT (uridine diphosphate glucuronyl transferase) to mono and diglucoronides, which are then excreted into bile canaliculi.

Enterohepatic Circulation Meconium contains 100-200mg of conjugated bilirubin at birth. Conjugated bilirubin is unstable and easily hydrolyzed to unconjugated bilirubin.
52

This process occurs non-enzymatically in the duodenum and jejunum and also occurs in the presence of beta-glucuronidase, an enteric mucosal enzyme, which is found in high concentration in newborn infants and in human milk.

Conjugation Since conjugated bilirubin crosses the placenta very little, conjugation is not active in the fetus with levels of UDPGT about 1% of adult levels at 30 - 40 weeks gestation After birth, the levels of UDPGT rise rapidly but do not reach adult levels until 4-6 weeks of age. Ligandins, which are necessary for intracellular transport of bilirubin, are also low at birth and reach adult levels by 3-5 day.

RISK FACTORS FOR SIGNIFICANT JAUNDICE Gestational Age Race Family history of jaundice requiring phototherapy Hemolysis (ABO or other) Severe bruising Breastfeeding ETIOLOGICAL CONSIDERATINS A. CLASIFICATION BASED ON TIME OF ONSET FIRSTDAY Rh and ABO incompatibilities Intrauterine infections like TORCH G-6-PD deficiency Hereditary spherocytosis Homozygous alpha-thalassemia SECOND AND THIRD DAY

53

Physiologic Hyperbilirubinemia of newborn Birth asphyxia Cephalohematoma Acidosis Hypothermia Hypoglycemia Drugs FOURTH TO SEVENTH DAY Septicemia Syphilis Toxoplasmosis Extra hepatic atresia of bile duct Breast milk jaundice AFTER FIRST WEEK Septicemia Extra hepatic atresia of bile duct Neonatal hepatitis Drug induced hemolytic anemia Galactosemia PERSISTANT JAUNDICE DURING FIRST MONTH OF LIFE Inspissated bile syndrome Cretinism Congenital hypertrophic pyloric stenosis B. CLASSIFICATION BASED ON CONJUGATION OF BILIRUBIN Increased production of bilirubin Hemolytic disease of the newborn Increased enter hepatic circulation Decreased clearance of bilirubin Inborn errors of metabolism Medications: vitamin K

54

Hormones: breast milk jaundice, hypothyroidism, hypopitutarism.

CLINICAL EXAMINATION OF JAUNDICE

Originally described by Kramer, dermal staining of bilirubin may be used as a clinical guide to the level of jaundice. Dermal staining in newborn progresses in a cephalo-caudal direction. The newborn should be examined in good daylight. The skin should be blanched with digital pressure and the underlying color of skin and subcutaneous tissue should be noted. Newborns detected to have yellow discoloration of the skin beyond the thighs should have an urgent laboratory confirmation for levels of bilirubin. Clinical assessment is unreliable if a newborn has been receiving phototherapy and if the baby has dark skin. Guide to dermal staining with level of bilirubin Area of body Level of bilirubin Face Chest, upper abdomen Lower abdomen, thighs Arms, lower legs Palms, soles 4-6 mg/dl 8-10 mg/dl 12-14 mg/dl 15-18 mg/dl 15-20 mg/dl

MEASUREMENT OF JAUNDICE Biochemical: Laboratory estimation of total and conjugated bilirubin based on Vanden Bergh reaction remains the gold standard for bilirubin estimation..
55

Bilimeter: It is based on spectro-photometry and estimates total serum bilirubin. It is useful in neonates, as bilirubin is predominantly unconjugated. Transcutaneous bilirubinometer: This method is non invasive and based on the principle of multi-wavelength spectral reflectance from the bilirubin staining in the skin. Variations due to skin thickness and pigmentation may interfere with the accuracy of the Instrument.

TYPES OF JAUNDICE Physiological jaundice Pathological jaundice Breast milk jaundice Breast feeding jaundice

PHYSIOLOGICAL JAUNDICE

Jaundice attributable to physiological immaturity usually appears between 24-72 hours of age, peaks by 4-5 days in term and 7th day in preterm neonates and disappears by 10-14 days of life. It is predominantly unconjugated and levels usually do not exceed 15 mg/dl. This pattern of physiological jaundice has been described in predominantly artificially fed babies. Based on recent recommendations of AAP, bilirubin levels upto 17-18 mg/dl may be accepted as normal in term healthy newborns. Safe bilirubin levels in preterms vary according to gestational age.

Possible mechanism of physiological jaundice Increase bilirubin load on liver cells Increased erythrocyte volume Increased enterohepatic circulation of bilirubin Increased erythrocyte survival Defective hepatic uptake of bilirubin from plasma Decreased ligandin Decreased hepatic uptake
56

Defective bilirubin conjugation Decreased UDPG activity Defective bilirubin excretion

Exaggerated physiological jaundice Certain common occurrence in newborn may increase the level of physiological jaundice, which may be prolonged and even require treatment. PATHOLOGICAL JAUNDICE

Bilirubin levels that deviate from the normal range and requiring intervention would be defined as pathological jaundice. Appearance of jaundice within 24 hours, increase in serum bilirubin beyond 5 mg/dl/day, peak levels above the expected normal range, presence of clinical jaundice beyond 2 weeks and conjugated bilirubin (dark urine staining the clothes) would be categorized under pathological jaundice. Causes of pathological jaundice Increased production Fetomaternal blood group incompatibility Non spherocytic hemolytic anemia Sepsis Increased enterohepatic circulation Decreased clearance Inborn errors of metabolism Drugs and hormones

BREAST-FEEDING AND JAUNDICE Exclusively breast-fed infants have a different pattern of physiological jaundice as compared to artificially fed babies2,3. Jaundice in breast-fed babies usually appears between 2472 hours of age, peaks by 5-15 days of life and disappears by the third week of life. They have also been reported to have higher bilirubin levels. One third of all breast-fed babies are detected to have mild clinical jaundice in the third week of life, which may persist into the 2nd to 3rd
57

month of life in a few babies. This increased frequency is not related to characteristics of breast milk but rather to the pattern of breast-feeding. Decreased frequency of breast-feeding is associated with exaggeration of physiological jaundice. Encouraging a mother to breastfeed her baby at least 10-12 times per day would be helpful in the management of jaundice in a term healthy baby.

BREAST MILK JAUNDICE

Approximately 2-4% of exclusively breast-fed term babies them have jaundice in excess of 10 mg/dl in the third week of life. These babies with serum bilirubin beyond 10 mg/dl in the third week of life should be investigated for prolonged jaundice. A diagnosis of breast milk jaundice should be considered if the serum bilirubin is predominantly unconjugated, other causes of prolonged jaundice have been excluded and the infant is in good health, vigorous and feeding well and gaining weight adequately. Mothers should be advised to continue breast-feeding at more frequent intervals and bilirubin levels usually subside over a period of time. Interruption of breast-feeding is not recommended unless levels exceed 20 mg/dl. SEQUELAE OF UNCONJUGATED BILIRUBIN Unconjugated bilirubin may penetrate brain cells under certain circumstances and result in neurologic dysfunction and even death. Transient encephalopathy Early bilirubin induced neurologic dysfunction is transient and reversible. This is suspected by increasing lethargy with rising bilirubin levels but recovery following or prompt exchange transfusion. Kernicterus This includes staining and necrosis of neurons in the basal ganglia, hippocampal cortex, subthalamic neuclei and cerebellum followed by gliosis of these areas. The cerebral cortex is generally spared, but 50% of babies have extra neuronal lesions with necrosis of renal tubular

58

cells, intestinal mucosa and pancreatic cells. These may manifest as gastrointestinal hemorrhage or hematuria. Kernicterus is described in phases and may progress over 24 hours to 7 days. Phase 1: poor suck, lethargy, hypotonia, depressed sensorium. Phase 2: fever, hypertonia progressing to opisthotonus. Phase 3: high pitched cry, convulsions, death. Long term complications include cerebral palsy, upward gaze palsy, sensory neural hearing loss and mental retardation. DIAGNOSIS

Serum Bilirubin : Total and direct Blood grouping and Rh typing of mother and baby: detect any incompatibility Direct coombs test of babys blood: detects presence of antibody coating on fetal RBC Peripheral smear for RBC morphology and reticulocyte count: evidence of hemolysis Hematocrit: decreased in hemoysis Sepsis screen G6PD screen Liver function test Thyroid screen TORCH titre In Rh iso immunized mothers Cord blood is screened for TSB Hematocrit, Blood Grouping and Rh typing and DCT.

PREVENTION OF HYPERBILIRUBINEMIA

-D immunoglobulin to Rh-ve mother

59

TREATMENT OF HYPERBILIRUBINEMIA

Treatment of hyperbilirubinemia is required to prevent CNS toxicity and thus bilirubin encephalopathy. The treatment decission depends on the followings .

vel of Jaundice The various treatment modalities include

TREATMENT GUIDELINES (according to AAP)

Age in hours Consider Phototherapy

Total Serum Bilirubin level, mg/dL Phototherapy Exchange transfusion if Intensive Phototherapy^ fails

Exchange transfusion and Intensive Phototherapy

<= 24 25-48 49-72 >72 12 15 17 15 18 20 20 25 25 25 30 30

Phototherapy at these TSB levels is a clinical option that many are used on the basis of individual clinical judgment. Term infants that are clinically jaundice at <=24 hours old are not considered healthy
60

PHOTOTHERAPY Phototherapy is found to be effective in treating jaundice in neonate. Unconjugated bilirubin in skin gets converted in to water-soluble, nontoxic photoproducts on exposure to light of a particular wave length (425-475mm) and is excreted in intestine and urine. There is no role for prophylactic phototherapy.

Mode of action

1. Geometric photoisomerization: of unonjugated bilirubin resulting in a more soluble form of bilirubin resulting in a more soluble form of bilirubin. This accounts for 80% of conversion.

2. Converting bilirubin to lumirubin through structural isomerization, which can then be excreted into the bile without the need for further hepatic conjugation.

3. Oxidation mechanism resulting in colorless by products and excreted by liver and kidney without need for conjugation. This is the least important mechanism.

Indication Used when the bilirubin level is hazardous to the to the infant, even though it is not reached at the exchange transfusion level. Prophylactic phototherapy incase of low birth weight or severely bruised infants.

Technique

Bilirubin absorbs light maximally in the blue range (420-500nm). Day light and cool white lamps have a spectral peak between 550-600nm and are less effective than special blue lamps, which have a range of 420-480nm. Blue lamps interfere with observation of skin color in the baby and cause headache and nausea to the care giver. Hence a combination of white and blue lamps is preferred. With prolonged use the irradiance of fluorescent lights tends to diminish,
61

hence light bulbs are preferably changed every 2000 hours. Distance of the baby from light sources affect the effectiveness of the treatment, a distance of 15-30cm used to be followed. Eyes must be shielded with eye patches to prevent potential adverse effect on retina and babies are kept naked, except for diapers, as larger the surface area exposed, more effective is the phototherapy. The efficacy of phototherapy depends upon (a) Surface area exposed to phototherapy. Double surface phototherapy may be more effective than single surface phototherapy. (b) Spectrum of light source: Special blue tubes with the mark F20T12/BB should be used rather than F20T12/B lights. (c) Irradiance or energy output may be increased in a phototherapy unit by decreasing the distance to within 15-30 cm of the infant. Continuous phototherapy is better than intermittent phototherapy. Phototherapy should be interrupted in a newborn only during breast-feeding and nappy changes.

Complications Increase in environment and body temperature: Phototherapy can cause increase in insensible loss of water and stool tend to be more loose and frequent. This can be compensated by increasing the fluid intake by 20ml/kg body weight. There should be a regular measurement of temperature and weighed twice daily. Retinal damage: studies indicate that retinal degeneration may occur after several days of continuous exposure. Bronze baby syndrome: the skin, urine and serum become brownish black after several days of phototherapy. Recover after therapy is discontinued. Electric shock

EXCHANGE TRANSFUSION

Introduction: This procedure, used most commonly to treat severe unconjugated hyperbilirubinemia, removes the infants circulating blood and replaces it with donor blood. The amount of blood exchanged is expressed as multiples of the infants blood volume. The standard two volume ExTx uses a
62

volume twice the infants blood volume (i.e., 170 mL/kg). The procedure is done in small increments. As the procedure progresses, relatively more of the donor blood (infused earlier) and less of the patients own blood is removed. The washout of the infants blood is a simple exponential function:

Volume exchanged (of patients total blood volume) 0.5 volume 1.0 volume 2.0 volume 4.0 volume

Patients blood removed (% of total blood volume) 39 % 63 % 86 % 98 %

INDICATION

Sickle cell disease Thrombotic thrombocytopenic purpura (TTP) Hemolytic disease of the newborn

The procedure involves slowly removing the patient's blood and replacing it with fresh donor blood or plasma. These values are for washout of the vascular compartment. However, an ExTx will remove more bilirubin than shown above. This is because unconjugated bilirubin is distributed in both the intra-vascular and extra-vascular spaces, and will move rapidly into the intra-vascualr space as the concentration decreases during the ExTx. Thus, a 2 volume ExTx will remove twice as much bilirubin as was in the circulating plasma at the start of the procedure. However, because of continued movement of bilirubin into the vascular space, the plasma bilirubin concentration at the end of the ExTx will be reduced by only of the pre-exchange level. PROCEDURE: Donor blood should be It should be fresh (less than 3 days old) Amount needed is double the blood volume (160ml/kg) Blood should be slowly warmed to infants temperature
63

Method and types of catheters: A. Continuous Exchange is performed by two operators, one infuses blood and the other simultaneously withdraws it. The best method is Withdrawal from an umbilical arterial catheter (UAC) and infusion into an umbilical venous catheter (UVC) with tip in IVC or right atrium. Flush withdrawal catheter with heparinized saline every 10-15 min to prevent clotting. Alternatives are: Withdrawal from a peripheral arterial catheter and infusion into a central venous catheter. However, this is slow and the arterial catheter frequently clots. Withdrawal from a central venous catheter and infusion into a peripheral vein. Flush the central catheter frequently to prevent clotting.

B. Push-Pull Method can be done through: A single UVC with tip in IVC or right atrium. A single UAC with tip in lower aorta (below 3rd lumbar vertebra) Caution: Do not perform ExTx through a UVC if the tip is in the portal circulation. Volume N.B: Blood Volume = 70-90 ml/kg for term and 85-110 ml/kg for preterm infants

One blood volume removes 65% of babys red cells. Two blood volumes removes 88% Thereafter the gain is small.

64

<1000gms 1000-2000gm >2000gm

Use 5ml aliquots 10ml 15ml

2. Technique: With the push-pull method, use increments of 5 mL/kg. Small increments are safer and just as efficient as larger ones, provided that you clear the donor blood from the dead-space of the catheter. Do this at the end of each infusion increment by withdrawing 2 mL of blood from the catheter into the syringe and then reinfusing it. During the procedure, the operator(s) must call out the volume in and out with each infusion and withdrawal (e.g. ten in - ten out). A 3rd person must keep a written timed, running record of each infusion and withdrawal and of cumulative volumes to be sure that the volumes infused and withdrawn are equal. Take 45-60 min to perform a 2 volume ExTx in a vigorous baby and longer in a sick one. If the infant is receiving O2 or assisted ventilation, measure pH, PaCO2 and PaO2 frequently (e.g., q 100 mL). You often will need to increase FIO2 during the ExTx. 3. Important reminders: Monitor ECG, blood pressure, O2 saturation, transcutaneous CO2 and temperature during ExTx. Measure pH at mid-point and at end of ExTx (more frequently in a sick baby. Measure glucose and electrolytes at end of ExTx, and glucose at 10, 30, 60 min later. Warm blood to 34-35 C. Warming blood to >37 C causes hemolysis. Agitate the unit of donor blood q 10-15 min so that cells do not settle. ExTx does not significantly plasma gentamycin level; do not give an extra dose.

COMPLICATIONS Problem with Donor Blood Blood is cold Effect on Infant Hypothermia Warm donor blood to 34 - 35o C High K+ Hyperkalemia, Use fresh blood, monitor ECG Prevention or Treatment

65

Arrhythmia Low pH (e.g., 6.9) Acidosis Consider buffering blood with THAM if infant is unstable. This will also [K+]. Consider platelet Tx at end of ExTx. If risk of bleeding, also Tx platelets at mid-point. Give 30 mg/kg of dilute Ca gluconate, over 5 min at , , and at end of a 2 volume ExTx, and if unexplained tachycardia or arrhythmia occurs. Start IV glucose at 5mg/kg/min 10-15 min after end of ExTx; monitor blood glucose.

No platelets (old blood or PRBC+FFP)

Thrombocytopenia

Citrate anticoagulant

Low Ca++ & Mg++

High glucose

Reactive Hypoglycemia

NURSING DIAGNOSIS Risk for hyperthermia related to phototherapy Risk for fluid volume deficit related to phototherapy Altered family process related to prolonged hospitalization Risk for infection related to invasive procedures.

66

NECROTIZING ENTEROCOLITIS
Necrotizing enterocolitis is an acute inflammatory disease of the bowel and death of intestinal tissue. It most often affects premature babies. CAUSES Necrotizing enterocolitis occurs when the lining of the intestinal wall dies and the tissue falls off. The cause for this disorder is unknown. However, it is thought that a decrease in blood flow to the bowel keeps the bowel from producing mucus that protects the gastrointestinal tract. Bacteria in the intestine may also be a cause. Those with a higher risk for this condition include:

Premature infants Infants who are fed concentrated formulas Infants who have received blood exchange transfusions RDS: prolonged periods of RDS causes hypoxia to all organs, thus intestinal part gets necrosed and when baby is starts with oral feeds, signs and symptoms of RDS occurs.

PATHOLOGICAL CHANGES Decreased blood supply to the bowel Cell death Stop secreting protective, lubricating mucus Bowel is attacked by proteolytic enzymes Bowel wall continues to swell and break down Unable to synthesis protective immunoglobulin M Mucosa permeable to macromolecules (exotoxins) Gas forming areas invade damaged areas and produce pneumatosis intestinalis, the presence of air in the submucosal or subserosal surfaces of the bowel

67

SYMPTOMS Symptoms may come on slowly or suddenly, and may include:

Abdominal distention Blood in the stool Diarrhea, vomiting Feeding intolerance Lethargy Temperature instability Hematemesis.

The clinical features are divided into 3 stages: Stage 1 Apnea, bradycardia, lethargy, abdominal distension and vomiting. Stage 2 Pneumatosis intestinalis and the above features. Stage 3 Low blood pressure, bradycardia, acidosis, disseminated intravascular coagulation (DIC) and anuria DIAGNOSTIC EVALUATION Radiographic studies: sausage shaped dilation of intestine, soapsuds- bulby appearance of thickened bowel wall. Lab findings: anemia. Leucopenia, metabolic acidosis, electrolyte imbalance, thrombocytopenia.

68

THERAPEUTIC MANAGEMENT

Withhold oral feedings for 24-48 hours. Minimal enteral feedings- (trophic feeding, gastrointestinal priming). Trophic feeding is the practice of feeding minute volumes of enteral feeds in order to

stimulate the development of the immature gastrointestinal tract of the preterm infant. Trophic feeding alters gastrointestinal disaccharidase activity, hormone release, blood flow, motility and microbial flora. Clinical benefits appear to include improved milk tolerance, greater postnatal growth, reduced systemic sepsis and shorter hospital stay. There is currently no evidence of any adverse effects following trophic feeding.

Abdominal decompression through NG suctioning. IV antibiotics. Correction of extravascular volume depletion. Correction of electrolyte abnormalities, acid base balance, hypoxia.

NURSING CONSIDERATION

Monitor vitals- changes may indicate bowel perforation Avoid taking rectal temperatures because of the risk of perforation Avoid pressure on the distended abdomen by left the baby undiapered and position on the side.

Strict hand washing.

69

NEONATAL SEIZURES INTRODUCTION Seizures are the most distinctive manifestation of neurologic dysfunction in the newborn infant. Although not life threatening as an isolated entity, seizures constitute a medical emergency because they signal a disease process that may produce irreversible brain damage. DEFINITION Convulsions are abnormal electrical discharges in the brain resulting in abnormal involuntary, paroxysmal, motor, autonomic or sensorial activity. INCIDENCE term babies- 0.5-0.8% preterm- 6-12% 5% of children experience convulsion in the 1st year of life. TYPES OF SEIZURE
subtle seizure

multifocal clonic seizures without jacksonian pattern focal clonic seizures tonic seizures myoclonic seizures

Subtle seizures Most common subtype, comprising about 50% of all seizures .It is common in preterm. Subtle seizures include a broad spectrum of behavioral phenomena, occurring in isolation or in combination. Features
Ocular phenomena are common. Jerking of eyes, tonic eye deviation.s Blinking or fluttering of eyelids. 70

Staring look, nystagmoid eye movements. Tachycardia followed by bradycardia Oro-bucco-lingual movements include chewing, sucking or lip-smacking movements and are often associated with a sudden increase in drooling.

Apneic attacks, sudden change in skin color. Various alternating limb movements include pedaling, boxing, rowing or swimming movements. Autonomic phenomena including sudden changes in skin color and capillary size, may occur alone or in combination with various motor manifestations.

Most subtle seizures are not associated with EEG seizures. Inconsistent association with EEG seizures and poor response to conventional anticonvulsants makes subtle seizures to be nonepileptic brain stem release phenomena. Clonic seizures These are stereotypic and repetitive biphasic movements with a fast contraction and a slower relaxation phase. Clonic seizures may be unifocal, multifocal or generalized. Clonic seizures that remain unifocal are usually not associated with LOC. The most common cause for clonic seizures that remain unifocal is neonatal stroke. Multifocal clonic seizures tonic convulsive movements migrate from one limb to another. twitching movements-limited to one side, cause: hypoxic ishchemic encephlopathy and birth trauma.

Focal clonic seizures Well localized. Associated with loc.

Causes include metabolic disorder, birth trauma and cerebral infarction Tonic seizures Have a sustained period (seconds) of muscle contraction without repetitive features. This may be generalized or focal. Generalized tonic seizures, which may closely mimic decerebrate or decorticate posturing, are most common in premature infants with diffuse neurologic dysfunction or major intraventricular hemorrhage (IVH).

71

Generalized tonic seizures are often associated with other motor automatisms or with clonic seizures as well. It is precipitated by tactile or other stimuli and may be abolished by repositioning or light restraint.

EEG pattern tend to have multifocal or generalized voltage depression and, in some cases, a markedly abnormal burst suppression pattern. Prognosis is very poor.

causes:
Early neonatal period

Birth asphyxia ICH Hypoglycemia Hypocalcaemia Pyridoxine dependency Dysnatremia IEM Difficult, obstructed labour. Maternal withdrawl of medications. neonatal period: hypocalcemia hypomagnesemia hypoglycemia dyselectrolytemia kernicterus microcephaly meningitis tetanus neonatorum septicemia metabolic errors:
72

PKU galactosemia Maple syrup urine disease miscellaneous conditions Neonatal narcotic withdrawal. drug toxicity Local anesthetics.

Myoclonic seizures These are distinguished from clonic seizures by their lightning fast contractions and nonrhythmic character. These seizures occur in a multifocal or generalized pattern. Usually associated with poor long term outcome.
Irregular or erratic in nature. In some cases it may be elicited by tactile or auditory stimulation or suppressed by restraint. Myoclonic contraction is usually associated with single high voltage spike and followed by a slow-wave complex.

Causes
Myoclonic seizures are associated with diffuse and serious brain dysfunction. Perinatal asphyxia IEM. Brain trauma. Cerebral dysgenesis.

73

Difference between Seizure and Jitteriness. Features Eye deviation/other ocular manifestation Stimulus sensitive Dominant Movement Movement ceases with gentle passive flexion EEG Seizure Present Jitteriness Absent

No Clonic jerking No

Yes Tremor Yes

Abnormal

no

SEIZURE MIMICS In the newborn it may be difficult to distinguish between normal immature behaviors (eg: nonnutritive sucking), abnormal but non-epileptic behaviors (eg: jitteriness), and true epileptic manifestations. The following guidelines help distinguish true epileptic seizures from seizure mimics. Epileptic apnea in the newborn Rare manifestation during neonatal seizure. It is difficult to distinguish from apnea due to other causes. Neonatal epileptic apnea rarely last longer than 10-20 seconds. True epileptic seizures are:
Rarely stimulus sensitive. Cannot be abolished by passive restraint or repositioning of the infant. Often associated with autonomic changes or ocular phenomena.

Benign neonatal sleep myoclonus

Relatively common and sometimes dramatic nonepileptic forms of myoclonus. This condition present in the first week of life, and resolves spontaneously over weeks to months.

74

Convulsive activity emerges during quiet non rapid eye movement (non-REM) sllep and is rapidly abolished by arousal. Precipitated in some cases by gentle rhythmic rocking or tactile stimuli, and gentle restraint may actually increase rather than abolish the myoclonus. These events never occur during wakefulness and the neurologic examination is normal. Immediately before and during the episodes, the EEG shows features of quiet sleep with no ictal changes. Anticonvulsants are not indicated, and, in fact benzodiazepines may exacerbate the myoclonic jerks. Long term outcome is normal and later epilepsy does not develop.

ETIOLOGIES OF NEONATAL SEIZURE Etiology

1. Cerebral hypoxia-ischemia a. Perinatal asphyxia b. Focal infarction (arterial venous) 2. ICH 3. CNS infection 4. Metabolic disease a. Transient b. IEM 5. Cerebral dysgenesis 6. Neonatal epileptic syndromes 7. Neonatal abstinence syndrome 8. Unknown

Incidence (%)

40
or 15

15 5 5 1 5 1 1s 10

a. Hypoxic ischemic encephalopathy

The leading cause of neonatal seizure is cerebral hypoxia-ischemia, which may occur in the antenatal, intrapartum or neonatal period. Most postasphyxial seizures in the newborn occur within the first 24 hours after the insult, 50% or more occurring within 12 hours of birth.
b. Focal ischemic injury

75

Neonatal arterial stroke: Occurs in around 1 in 4,000 live births. Seizures are the most common presentation of stroke in the newborn period, and stroke is the second most common cause of neonatal seizures. Cerebral vein thrombosis: Lethargy is often the only feature, approximately 60% of cases develop neonatal seizures. Here, infants will be more encephalopathic, with depressed mental status before and between seizures.
c. ICH Implicated in 10% of neonatal seizures. Infants with seizure associated with primary SAH have a good long term outcome in 90% of cases. d. CNS infections CNS infections from a variety of agents, including viral, bacterial or other organisms such as toxoplasmosis, may have neonatal seizures as a prominent part of their presentation. These infections may originate in the fetus, for example, congenital encephalitis due to CMV and toxoplasmosis. Other causes include herpes simplex virus, streptococcal infection, E.Coli. e. Metabolic disturbances 2 types are there: transient and rapidly correctable disturbances; inherited and usually persistent causes.

Transient Metabolic disturbances: Include disturbances of blood glucose and electrolyte disturbances such as hypoglycemia, hypocalcaemia and hypomagnesaemia.
Hypoglycemia Common in infants with IUGR, diabetic mothers or perinatal asphyxia, galactosemia, hyperinsulinemic conditions (eg. Beck-With-Wiedeman syndrome). Because seizures develop after sustained hypoglycemia, these infants often have a poor outcome. Hypocalcemia Accounts for approximately 3% of neonatal seizures. Hyponatremia May develop in the setting of inappropriate ADH secretion , perinatal aasphyxia and inadvertent water intoxication. 76

IEM Uncommon cause of neonatal seizures. It includes:

Pyridoxine dependency

Pyridoxine dependency results from impaired binding of the active form of pyridoxine to the enzyme glutamic acid decarboxylase (GAD).

Normally, Glutamate (excitatory amino acid neurotransmitter)

GAD

GABA (inhibitory neurotransmitter).

Impaired GAD activity causes marked increase in excitatory neurotransmitter levels and this precipitate seizure. Affected infants have low GABA levels and high glutamate levels in the CSF. Seizure cease after appropriate dose of pyridoxine. Pyridoxine :
Dose : 50-100 mg IV Pyridoxine administration increases the cerebral synthesis of the inhibitory transmitter GABA, apnea and hypotonia may occasionally develop, necessitating close respiratory monitoring.

Glycine encephalopathy (nonketotic hyperglycinemia) It is an autosomal recessive condition which tresults in very high levels of glycine in the brain

and CSF, which results in refractory myoclonic seizures, stupor, respiratory disturbances and hypotonia. Most infants with nonketotic hyperglycinemia die by 1 year of age.

77

STATUS EPILEPTICUS (SE) SE implies prolonged single seizure or multiple episodes of seizures lasting more than 30 minutes without regaining consciousness in between. Types of status epilepticus: Convulsive Non- convulsive.

INVESTIGATIONS FOLLOWING NEONATAL SEIZURE 2nd line 1 line Pulse oximetry Glucose Packed cell volume Sr. Calcium, Sodium, Magnesium Lumbar Puncture Blood Culture Cranial USG. EEG Arterial pH CT Specimens for detecting congenital infections Urinary amino acids Organic acids Therapeutic trial of pyridoxine.
st

GOALS OF THERAPY Ensure adequate vitals, systemic and cerebral oxygenation. Terminate seizure activity. Prevent seizure recurrence. Establish diagnosis and treat underlying disorder.
78

calcium gluconate: 200mg/kg magnesium sulphate: 0.2ml/kg glucose: 5-10 ml/kg Maintain blood glucose between 70-120 mg/dl. anticonvulsant therapy
First drug of choice is diazepam(DZP) 0.1MG/KG increasing slowly up to 0.3 mg/kg. Lorazepam (LZP): 0.05mg/kg IV- repeat to a total dose of 0.1mg/kg. Phenobarbitol: 20mg/kg IV over 10-15 minutes. If seizure persist, further bolus of 5mg/kg, up to a total dose of 40 mg/kg or control of seizures. Fosphenytoin: 20mg/kg IV at 1mg/kg/mt If seizure persist, an additional dose of 5mg/kg can be given. Maintenance= 5-8 mg/kg/mt.

This need to be diluted in 5%D.

Midazolam: 0.02-0.1 mg/kg IV stat followed by 0.01-0.06 mg/kg/hr continues infusion. Pyridoxine: 100mg IV/PO Maintenance: 100mg/day. Folinic acid: start at 2.5 mg BD PO; increase up to 8mg/kg/day. Liveracetam: 10 mg/kg IV OD Clobazam: 0.25-1 mg/kg/day.

79

NURSING CARE OF HIGH-RISK NEWBORN IN GENERAL

Respiratory support Positioning Oxygen and associated ventilation

Thermoregulation Mummify the baby Kangaroo care Fabric insulated or wool cap Heated gel mattress with radiant heat Automatically controlled/ servo controlled incubators: the servo control is usually set to a desired skin temperature between 36 and 36.5 degree C. Radiant warmer/ incubator Open bassinet with cotton blankets. Double walled incubators: improves the infants ability to maintain a desirable temperature and reduce energy expenditure related to heat regulation. A number of micro enviroments may be used with the VLBW and ELBW infant to minimize evaporative and insensible water loss. These include items such as thermal blankets or plastic wrap, humidified reservoirs for incubators, and humidified plastic heat shields covered with plastic wrap. Protection from infection Meticulous, frequent hand washing Follow standard precautions in NICU. Restrict visitors. Regular cleaning of the equipments used in the care of infants.

80

Hydration Supplemental parenteral fluids are needed to supply additional calories, electrolytes or water. Nurses should be constantly alert for signs of IV infiltration ( erythema, edema, color change of tissue, blanching at site) and for signs of over hydration ( weight gain of more than 30 g in 24 hours, periorbital edema, tachypnoea and crackles on lung auscultation.

Nutrition Breast feeding Gavage feeding: safe means of meeting the nutritional needs or infants who are younger than 32 weeks of gestation or weigh less than 1500g. Through parenteral or enteral route. IV fluids specially designed to meet the infants nutritional needs, including protein, amino acids, trace minerals, vitamins, carbohydrates and fat (lipid emulsion). Skin care Initial bath: use cleansing agents with neutral pH. DO NOT completely remove venix Bath preterm infant less than 32 weeks in sterile water only. Emollients Adhesives: decrease the use as much as possible, use hydrogel or limb electrodes. Antiseptic agents

81

Trans epidermal water loss( TEWL): minimize TEWL and heat loss in small premature infants less than 30 weeks by measuring ambient humidity during first week of life, emollient application, servo- controlled humidifying incubator.

Preventing skin breakdown Decrease pressure from externally applied forces; apply transparent adhesive dressings to arms, elbows; use emollient in the diaper area to reduce urine irritation.

Treating diaper dermatitis. Maintain clean, dry skin Use absorbent diapers and change often. If mild irritation occurs, use petrolatum barrier. For severe dermatitis, identify cause and treat.

Developmental care Infants eye should shield from bright procedure lights to prevent potential harm. Skin- to-skin (STS) contact or kangaroo care

International Journal of Epidemiology , Vol 39 Aug 2012 states that KMC substantially reduces neonatal mortality amongst preterm babies less than 2000g in hospitals and is highly effective in reducing severe morbidity particularly from infection. Co- bedding of twins is another developmental intervention that has recently been implemented in the institutions of United States to provide a better environment for neonatal growth and development.
82

Family support and involvement Facilitating parent-child relationships.

NURSING CARE PLAN OF HIGH RISK NEW BORN IN GENERAL

1. Ineffective breathing pattern related to pulmonary and neuromuscular immaturity Interventions: Assess the respiratory status of the baby Position for optimal air exchange Avoid neck hyperextension Observe for signs of respiratory distress. Suction to remove accumulated mucus from nasopharynx, trachea, and endotracheal tube. Use semi prone or side-lying position to prevent aspiration. Close monitor blood gas measurements and Sao2 readings. Observe and assess babys response to ventilation and oxygen therapy.

2. Ineffective thermoregulation related to immature temperature control and decreased sub cutaneous body fat. Monitor temperature hourly. Place infant in incubator or radiant warmer. Regulate servo-controlled unit Use plastic heat shield as appropriate. Monitor for signs of hyperthermia.

3. Risk for infection related to deficient immunologic defences or inavasive procedures Ensure that all caregivers wash hands before and after handling baby. Ensure that all equipment in contact with the baby is clean. Prevent persons with upper respiratory tract or communicable infections from coming into direct contact with baby.
83

Isolate other infected babies. Administer antibiotics as per order.

4. Imbalanced nutrition: less than body requirement related to inability to ingest nutrients due to immaturity or illness. Maintain parenteral fluid or total parenteral nutrition therapy as ordered. Assess readiness to nipple feed Follow burping after each feed Follow unit protocol for advancing volume and concentration of formula. Assist mother with expressing breast milk. Assist mother with breast feeding.

5. Delayed growth and development related to preterm birth, separation from parents, physiologic immaturity. Provide optimum nutrition. Provide regular periods of undisturbed rest. Promote parent infant interaction.

CONCLUSION Improved perinatal and neonatal care has resulted in improved survival of many sick and small neonates who are risk for long term morbidities such as growth failure, developmental delay and visual/hearing problems. A proper and appropriate follow-up programme would help in prevention, early detection and appropriate management of these problems, thereby ensuring disability and morbidity free survival. REFERENCE Ghai OP, Paul V K, Bagga A. (2010). Ghai Essential Pediatrics. 7th ed. CBS Publishers and Distributers, India. Marlow, D.R; Redding B.A. (2010) . Text Book of Pediatric Nursing.(6th ed). India: Elsevier Publishers.

84

Hockenberry, Mj. Winkelstein. Wilson. (2005). Wongs Essentials of Pediatric Nursing. (7th ed). India: Elsevier Publishers. Ball,J W. Blinder RC (2009). Pediatric Nursing Caring for Children. ( 4TH ed). India:Pearson education publishers Assuma Beevi T M. (2012). Pediatric nursing care plans. 1st ed. Jaypee brothers publishers.

Lowdermilk DL. Perry s. (2006). Maternity Nursing. 7th ed. Mosby Elsevier Publishers. Canada. Dawn, C S. (2004). Text Book of Obstetrics and Neonatology. 16th ed. Dawn books. Kolkata. http://www.rcjournal.com http://ncbi.nlm.nih.gov/pubmed.
http://en.wikipedia.org/wiki/retinopathy_of_prematurity

http://www.google.co.in/imgres?hl=mwww.http://en.wikipedia.org/wiki/apnea_of_prema tur
Acta pediatrica,Volume 90, Issue Supplement s436,

http://www.ana.ed.ac.uk/anatomy/lungbase/lungdev.html
http://www.google.co.in/search?q=composition+of+surfactant&hl=en&prmd=imvns&sou

85