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High risk newborns and child during illness and hospitalization pediatric nursing

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DENNIS MUÑOZ
DENNIS MUÑOZ

High-risk newborns and child during illness and hospitalization pediatric nursing

Health & Medicine
1 of 200
HIGH RISK NEWBORN • High Risk Neonates  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 extrauterine existence.
HIGH RISK NEWBORNS • Encompasses human growth and development from the time of viability – 28 days following birth and includes threat to life and health that occur during the prenatal, perinatal, and postnatal periods. • Viability – gestational age at which survival outside the uterus is believed to be possible, or as early as 23 weeks of gestation.
CLASSIFICATION OF HIGH-RISK NEWBORN • Birth Weight • Gestational Age – preterm/post term • Predominant Physiologic Factors – associated with state of maturity; chemical disturbances (hypoglycemia, hypocalcemia); consequences of immature organ systems (hypothermia, Respiratory Distress Syndrome,
CLASSIFICATION ACCORDING TO SIZE • Low Birth Weight – less than 2500g regardless of gestational age • Moderately Low Birth Weight – birth weight is between 1501g to 2500g. • Very Low Birth Weight – birth weight is less than 1500g. • Extremely Low Birth Weight – birth weight less than 1000g.
CLASSIFICATION ACCORDING TO SIZE • Appropriate for Gestational Age (AGA) – birth weight falls between the 10th and 90th percentile • Small for Gestational Age (SGA) – birth weight falls below the 10th percentile • Large for Gestational Age (LGA) – birth weight falls above the 90th percentile
CLASSIFICATION ACCORDING TO GESTATIONAL AGE • Premature Infant – born before the completion of 37 weeks of gestation, regardless of birth weight • Full-Term Infant – born between the beginning of the 38 weeks and the completion of the 42 weeks of gestation • Postmature Infant – born after 42 weeks of gestational age, regardless of birth weight
PRETERM INFANTS • An infant born before term (</=36 weeks); premature or preterm • A low birth weight infant: </=1300-2000g (Philippine Standards) (,2.5kg) • Born before complete maturity; born before body and organ system have completely matured. • PRETERM: refers to pregnancy (PT labor); PREMATURE: to describe a baby
PRETERM INFANTS INCIDENCE: • Highest among low socio economic class • Largest # of admission to NICU • 12% of all pregnancies • Multiple pregnancies • PIH • Placental problems
PRETERM INFANTS CAUSES: • UNKNOWN • MATERNAL FACTOR • Malnutrition • Preeclampsia (toxemia of pregnancy) • Chronic Medial illness (Cardiac/kidney disease/DM) • Infection (UTI, vaginal infection) • Drug Use (coccaine, tobacco, alcohol) • Abnormal structure of the uterus • Previous PT Births
PRETERM INFANTS CAUSES: • PREGNANCY • Hypertension • Incompetent Cervix • Placental Previa/ Abruptio Placenta • PP.OM, poly/oligohydramnios • FETUS • Chromosomal abnormalities • Intrauterine Infection • Anatomic Abnormalities • IUGR, multiple gestations
PRETERM INFANTS DIAGNOSTIC EVALUATION: • Appraisal is made as soon as possible after admission to the nursery. • HEAD – head circumference is large in comparison with chest (reflects cephalocaudal direction of growth) • The fontanels are small and bones are soft • Soft cranium subject to characteristic nonintentional deformation, “preemie head” • Absent eyebrows, eyes closed, and ears are poorly supported by cartilage (soft and pliable) • Bones of skull and ribs – soft • Very small and appear scrawny – less subcutaneous fat (skin is wrinkled)
PRETERM INFANTS DIAGNOSTIC EVALUATION: • SKIN – bright pink (often transluscent) with small blood vessels • Smooth and shiny (may be edematous) with small blood vessels clearly visible underneath thin epidermis • Fine lanugo hair abundant over body, sparse, fine & fuzzy on head • Soles and palms – minimal creases • Harlequin color – Skin color changes when preterm infant is moved; upper half or one side of the body is pale or one side of the body is red. • Small breast bud size with underdeveloped nipples • Male Infants – few scrotal rugae, undescended testes
PRETERM INFANTS DIAGNOSTIC EVALUATION: • Labia and clitoris are prominent in females • Posture - complete relaxation with marked flexion and abduction of the thighs; random movements are common with slightest stimulus • Activity – Inactive and listless • Extremities maintain an attitude of extension and remain in any position in which they are placed. • Reflexes – partially developed • Sucking absent, weak or ineffectual; swallow, gag, cough reflexes – ABSENT • Temperature instability – Heat regulation poorly developed in the preterm infant because of poor development of CNS • Increased susceptibility to infection
PRETERM INFANTS DIAGNOSTIC EVALUATION: • Respirations are not efficient because of muscular weakness of lungs and rib cage and limited surfactant production; • Retraction at xiphoid is evidence of air hunger • Infants should be stimulated if apnea occurs • HMD/RDS, chronic lung disease, BPD, apnea of prematurity • Greater tendency toward capillary fragility in the preterm infant • Red and white blood cell counts are low with resulting anemia during first few months of life. • Neuro – Higher incidence of intracranial hemorrhage in the preterm infant • Muscle twitching, convulsions, cyanosis, abnormal respirations, and a short shrill cry • Cerebral palsy, visual-motor deficits, altered intellectual functions
PRETERM INFANTS DIAGNOSTIC EVALUATION: • GIT: Nutrition is difficult to maintain – because of weak sucking and swallowing reflexes, small capacity of stomach, and slow emptying time of the stomach • Renal: Reduced glomerular filtration rate results in decreased ability to concentrate urine and conserve fluid. • Higher ECF – vulnerable to fluid and electrolyte imbalance • Cardio: (+) murmur • More susceptible to biochemical alterations – hyperbilirubinemia, hypoglycemia • The greater degree of immaturity, the greater the degree of potential disability.
PRETERM INFANTS THERAPEUTIC MANAGEMENT: • Team approach: neonatologist, advance practice nurse, nurse staff, respiratory therapist • Incubator, IV lines, Oxygen therapy • PREVENTION: • PRENATAL CARE: key factor • Good nutrition and education • ID mothers at risk • Educate on symptoms of PT labor • Avoid heavy/repetitive work or standing long periods of time
PRETERM INFANTS THERAPEUTIC MANAGEMENT: • TREATMENT: • Oxygen, IVF • Umbilical catheterization – IVF, meds, bld extraction • X-ray • Special feedings of breastmilk/formula • Medications • Kangaroo care – shorter stay in NICU
PRETERM INFANTS THERAPEUTIC MANAGEMENT: • DISCHARGE: • Usually stay in hospital until reach pregnancy due date depending on their condition • GOALS: • Serious illness resolved • Stable temperature • Taking all feedings by breast/bottle • No recent apnea/bradycardia • Parents are able to provide care (meds and feedings) • Prior to discharge: eye examination, follow up visits
PRETERM INFANTS NURSING CARE: • IMPLEMENTATION: • Maintain airway; check respirator function if employed; position to promote ventilation; suction when necessary; maintain temperature of environment; administer oxygen only if necessary • Observe for changes in respirations, color, and vital signs • Check efficacy of Isolette: maintain heat, humidity, and oxygen concentration; monitor oxygen carefully to prevent retrolental fibroplasias • Maintain aseptic technique to prevent infection • Adhere to the techniques of gavages feeding for safety of the infant
PRETERM INFANTS NURSING CARE: • IMPLEMENTATION: • Observe weight-gain patterns • Determine blood gases frequently to prevent acidosis • Institute phototherapy by letting them verbalize and ask questions to relieve anxiety • Provide flexible and liberal visiting hours for parents as soon as possible • Allow parents to do as much as possible for the infant after appropriate teaching • Arrange follow-up before and after discharge by a visiting nurse or a Barangay Health Worker
POST MATURE INFANTS • After 42 weeks AOG/ 294 days past 1st day of mother’s LMP; regardless of birth weight • Post term, post maturity, prolonged pregnancy, post datism • INCIDENCE: • 7% (3.5-15%) OF ALL PREGNANCIES • CAUSES: unknown • History of >/= 1 previous post term pregnancies & miscalculated due date (not sure of LMP)
POST MATURE INFANTS FETAL RISK: • Progressive placental dysfunction – placenta (supplies nutrient & oxygen) ages toward the end of pregnancy --- may not function efficiently • Amniotic fluid volume decreases, fetus may stop gaining weight/ weight loss • Decreased amniotic fluid may lead to cord compression during labor • Increased risk of MAS and hypoglycemia • Increasing size (mainly length) & hardening of skull may contribute to CPD • GREATEST RISK: during stresses of labor & delivery especially in infants of primigravidas.
POST MATURE INFANTS CHARACTERISTICS OF INFANTS (1-3wks of AGE): • Absent lanugo, little if any vernix caseosa, abundant scalp hair, overgrown nails • Dry, peeling skin (cracked, parchmentlike & desquamating) • Wasted physical appearance (reflects intrauterine deprivation) • Minimal fat deposit (depleted subcutaneous fat) – thin, elongated appearance • Meconium staining – seen in skin folds w/ vernix caseosa • Visible creases palms/ soles
POST MATURE INFANTS DIAGNOSIS: P.E • UTZ, non-stress testing, estimate amniotic fluid volume MANAGEMENT: • Check respiratory problems related to meconium • Blood test for hypoglycemia • PREVENTION: • Accurate due date and UTZ • Cesarean section/ induction of labor - recommended
HYPERBILIRUBINEMIA • Refers to excessive level of accumulated Bilirubin in the blood • JAUNDICE or ICTERUS – yellowish discoloration of skin, sclera, nails • Relatively benign but it can also be pathologic
HYPERBILIRUBINEMIA PATHOPHYSIOLOGY: RBC DESTRUCTION Globin Heme Unconjugated Bilirubin liver Bilirubin detched from albumin through enzyme glucoronyl transferase + glucoronic acid Conjugated Bilirubin Excreted into Bile (feces and urine) Protein (used by the body)
HYPERBILIRUBINEMIA PATHOPHYSIOLOGY: • Result from increased unconjugated/ conjugated bilirubin • Bilirubin – one of the breakdown products of hgb from RBC destruction • Unconjugated Bilirubin – insoluble, bound to albumin • Intestines – (+) bacterial action – reduces conjugated bilirubin • Urobilinogen – pigment that gives stool its characteristic odor.
HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE CAUSE: Immature hepatic function + increased bilirubin load from RBC hemolysis Decreased milk intake related to fewer calories consumed by infant before mother’s milk is well established; enterohepatic shunting Possible factors is breast milk that prevent bilirubin conjugation Less frequent stooling Blood antigen incompatibility causes hemolysis of large # of RBCs. Liver unable to conjugate & excrete excess bilirubin from hemolysis COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE ONSET: After 24 hours (preterm infants, prolonged) 2nd – 4th day 5th – 7th day During 1st 24 hrs (levels increase faster than 5mg/ml/day) PEAK: 75 – 90 hours 3rd – 5th day 10th – 15th day Variable DURATION: Declines on 5th-7th day Variable May remain jaundiced x 3- 12 weeks or more Dependent on severity & treatment COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE THERAPY: Increase frequency of feedings & avoid supplements. Evaluate stooling pattern. Monitor Transcutaneous Bilirubin (TcB)/ Total Serum Bilirubin (TSB) Frequent (10-12x/day) breastfeeding, avoid glucose water, water supplements or formula. Evaluate stooling pattern; stimulate as needed. Increase frequency of breast feeding; use no supplementations (glucose water); cessation of breastfeeding not recommended. Perform risk assessment. Monitor TcB/TSB level. Perform risk assessment POST NATAL – phototherapy; administer IVIG per protocol; if severe, perform exchange transfusion. COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE THERAPY: Perform risk assessment. Use phototherapy if bilirubin level increases significantly (>5mg/dl/day) or significant hemolysis is present. Use phototherapy if bilirubin level increases significantly (17-22mg/dl) or significant hemolysis is present. Consider performing additional evaluations: G6PD, direct and indirect serum bilirubin, family history & others as necessary. PRENATAL – transfusion (fetus) Prevent sensitization (Rh Incompatibility) of Rh- negative mother with Rhig (Rhogam) COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE THERAPY: If phototherapy is instituted, evaluate benefits & harm of temporarily discontinuing breastfeeding; additional assessments may be required. Assist mother with maintaining milk supply, feed expressed milk as appropriate. After discharge, follow up according to hour of discharge. May include home phototherapy with a temporary (10-12hr) discontinuation of a breastfeeding; a subsequent TSB may be drawn to evaluate a drop in serum levels. Assist mother with maintenance of milk supply & reassurance regarding her milk supply and therapy. Use formula supplements only at practitioner’s discretion. PRENATAL – If mother is breastfeeding, assist with maintenance & storage of milk; may bottle-feed expressed milk as appropriate to therapy. Minimize maternal-infant separation & encourage contact as appropriate. COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA POSSIBLE CAUSES: • PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): • Physiologic Jaundice / Icterus Neonatorum – most common cause; no pathologic process 2 PHASES: term infants • 1ST phase – Bilirubin: 6mg/dl on 3rd DOL  decreased to 2-3mg/dl by 5th day • 2nd phase – Steady plateau without increase/decrease level  12th-14th day: levels decresed to normal (1mg/dl) • Pattern varies according to racial group, method of feeding, gestational age PRETERM: Bilirubin – 10-12mg/dl at 4-5days  slowly decrease by 2-4 weeks.
HYPERBILIRUBINEMIA POSSIBLE CAUSES: • PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): • Mechanisms Involved: • NB produce 2x as much bilirubin as do adults due to higher concentrations of circulating RBC & shorter life span of RBC (70-90days) • Liver’s ability to conjugate bilirubin reduced – due to limited production of glucoronyl transferase • Lower plasma binding capacity for bilirubin because of lower albumin concentrations than other children.
HYPERBILIRUBINEMIA POSSIBLE CAUSES: • PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): • Primary Mechanism : enterohepatic circulation/shunting • Normally: Conjugated bilirubin  urobilinogen (excreted) • Sterile & less motile NB bowel is less effective in excreting urobilinogen • Conjugated bilirubin thru B-glucoronidase converted back to unconjugated bilirubin reabsorbed by intestinal mucosa  liver
HYPERBILIRUBINEMIA POSSIBLE CAUSES: • An association with breast feeding or breast milk • BREASTFEEDING JAUNDICE – early onset • Begins at 2-4days of age; 12-13% of Breastfeeding infants • Related to process of breastfeeding, results from decreased caloric & fluid intake by Breastfeeding infants before milk supply is well-established (fasting is associated with decrease hepatic clearance of bilirubin) • Feeding (+) peristalsis  more rapid passage of meconium decreased amount of reabsorption of unconjugated bilirubin • Feeding introduces bacteria to aid in reduction of bilirubin to urobilinogen • Colostrums, natural cathartic, facilitates meconium evacuation
HYPERBILIRUBINEMIA POSSIBLE CAUSES: • An association with breast feeding or breast milk • BREAST MILK JAUNDICE – late onset • Onset: 4th-7th day of age; 12-13% of Breastfeeding infants • Rising levels peak at 2nd week  gradually diminish • May remain jaundiced x 3-12 weeks or more  infants are well • May be caused by factors in BM (pregnanediol, fatty acids, B-glucorinidase) that either inhibit conjugation or decrease excretion of bilirubin • Less frequent stooling by Breastfeeding infants may allow for extended time for reabsorption of bilirubin from stools
HYPERBILIRUBINEMIA POSSIBLE CAUSES: • Excess production of bilirubin – Hemolytic disease, biochemical defects, bruises • Hemolytic disease – blood antigen incompatibility – hemolysis of RBC ; liver unable to conjugate & excrete excess bilirubin from hemolysis • Onset: 1st 24 hours (levels increase faster than 5mg/dl/day) • Treatment: Postnatal – phototherapy ; exchange transfusion – severe • Prenatal – transfusion (fetus) ; Rhogam
HYPERBILIRUBINEMIA POSSIBLE CAUSES: • Disturbed capacity of liver to secrete conjugated bilirubin – enzyme deficiency, bile duct obstruction • Combined overproduction & undersecretion – sepsis • Some disease states – hypothyroidism, galactosemia, infant of a diabetic mother • Genetic predisposition to increase production – Native Americans, Asians
HYPERBILIRUBINEMIA CLINICAL MANIFESTATIONS • Jaundice – most obvious sign • Yellowish discoloration: sclera, nails, skin • If it appears within 1st 24 hours: hemolytic disease of Newborn, sepsis, maternally- derived diseases (DM, infections) • Appears on 2nd or 3rd day, peaks on 3rd – 4th day, declines on 5th – 7th day: physiologic jaundice (varies according to ethnicity) • Intensity of jaundice is not always related to the degree of hyperbilirubinemia
HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION • Serum Bilirubin (B1: 0.2-1.4mg/dl) • Jaundice appears at >5mg/dl • Evaluation based on: • Timing of appearance of clinical jaundice • Gestational age at birth • Age in days since birth • Family history including maternal Rh factor • Evidence of hemolysis • Feeding method • Infant’s physiologic status • Progression of serum bilirubin levels
HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION • Indicators of physiologic jaundice – warrants further investigation as to the cause of jaundice • Clinical jaundice within 24 hrs. of birth • Persistent jaundice over 2 weeks in full-term, formula fed infant • Total serum bilirubin levels 12.9mg/dl (term infant) or over 15mg/dl (preterm); upper limit for breastfeeding infant – 15mg/dl • Increase serum bilirubin >5mg/dl/day • Direct bilirubin (B2) 1.5-2mg/dl • Total serum Bilirubin – over 95th percentile for age (in hours) on hour-specific risk nomogram
HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION • Transcutaneous Bilirubinometry – noninvasive monitoring of bilirubin via cutaneous reflectance mechanisms; allow for repetetive estimations of bilirubin • Hour-specific Serum Bilirubin Levels – predict newborn at risk for rapidly rising levels • Recommended by AAP for monitoring healthy Newborn >35wks AOG before discharge from hospital • Carbon monoxide indices in exhaled breath – CO is produced when RBC is broken down
HYPERBILIRUBINEMIA COMPLICATIONS • BILIRUBIN ENCEPHALOPATHY/ KERNICTERUS – unconjugated bilirubin highly toxic to the neurons • Syndrome of severe brain damage due to deposition of unconjugated bilirubin in brain cells (extremely high B1 level increase crosses the blood-brain barrier) • KERNICTERUS – yellow staining of brain cells that may result in bilirubin encephalopathy
HYPERBILIRUBINEMIA COMPLICATIONS • FACTORS THAT CONTRIBUTE TO BILIRUBIN NEUROTOXICITY: • Serum bilirubin alone do not predict the risk of brain injury • Metabolic acidosis • Low serum albumin level • Intracranial infections (meningitis) • Abrupt increase in BP • Conditions that increase metabolic demands for oxygen and glucose – fetal distress, hypoxia, hypothermia, hypoglycemia
HYPERBILIRUBINEMIA COMPLICATIONS • SIGNS OF CNS DEPRESSION/ EXCITATION: • Prodrome: decreased activity, lethargy, irritability, hypotonia, seizures • Athetoid CP, mental retardation, deafness • Those who survived: NEUROLOGIC DAMAGE • Mental retardation, ADHD, delayed/ abnormal motor movements (ataxia, athetosis), behavior disorders, perceptual problems, sensorineural hearing loss
HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Phototherapy – main form • Exchange transfusion – reduce high bilirubin levels that occur with hemolytic disease • Phenobarbital – hemolytic disease; effective when given to mother several days before delivery • Promotes hepatic glucoronyl transferase synthesis  increases bilirubin conjugation & hepatic clearance of pigment in bile • Promotes protein synthesis – increase albumin for more bilirubin binding sites • Heme-oxygenase inhibitors – decrease bilirubin production
HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Early initiation of feedings & frequent breastfeeding – promotes increased intestinal motility, decreases enterohepatic shunting, establish normal bacterial flora in the bowel excrete B2 • Frequent breastfeeding every 2 hrs • Avoid glucose water, formula or water supplementation
HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Phototherapy – application of fluorescent light (bili light) to infant’s exposed skin • Light  promotes bilirubin excretion by photoisomerization (alters structure of bilirubin to a soluble form – lumirubin) for easier excretion • Blue Light – more effective in reducing bilirubin but alters the color of the infant • Fluorescent bulbs with spectrum 420-460nm preferred • Infant skin is fully exposed
HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Phototherapy – application of fluorescent light (bili light) to infant’s exposed skin • Rapidly rising bilirubin/ critical level – double intensive phototherapy • Conventional overhead lamps while infant is lying on fiber optic blanket • BEST RESULT: occur within 1st 24-48hrs of treatment • Fiberoptic blanket/panel – light generating illuminator • blanket delivers therapeutic light consistently & continuously to infant & achieve same photoisomerization as conventional phototherapy • For home phototherapy, permits more infant-parent interaction, better temperature control • Eliminates the need for eye patches • SPECIAL CAUTION: plastic pad must completely be covered to prevent exposing fragile skin of extremely immature/compromised infant to fiberoptic blanket (dermal injury) • When blood is drawn, phototherapy lights are turned off, blood is transported in covered tube to avoid false reading as a result of bilirubin destruction in test tube.
HYPERBILIRUBINEMIA AGE (HOURS) CONSIDER PHOTOTHERAPY PHOTOTHERAPY EXCHANGE TRANSFUSION IF INTENSIVE PHOTOTHERAPY FAILS EXCHANGE TRANSFUSION AND INTENSIVE PHOTOTHERAPY 24 --- --- --- --- 25-48 >/= 12 (170) >/= 15 (260) >/= 20 (340) >/= 25 (430) 48-72 >/= 15 (260) >/= 18 (310) >/= 25 (430) >/= 30 (510) >72 >/= 17 (290) >/= 20 (340) >/= 25 (430) >/= 30 (510) MANAGEMENT OF HYPERBILIRUBINEMIA IN HEALTHY TERM NEWBORN TSB LEVEL (mg/dl/mmol/L)
HYPERBILIRUBINEMIA PROGNOSIS: • Early recognition prevents brain damage • Bilirubin encephalopathy: athetosis, sensorineural hearing loss, paralytic gaze palsy, gaze abnormalities, delayed motor skills, dental enamel hypoplasia
HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • ASSESSMENT • Observe for evidence of jaundice at regular intervals • Observe color from head-toe, color of sclera & mucous membranes • Apply direct pressure to skin especially bony prominences (tip of nose or sternum)  blanching  allow yellow stain to be more pronounced • Dark-skinned – color of sclera, conjunctiva, oral mucosa • Observe natural daylight • Evidence of jaundice that appears before infant is 24 hrs of age – indication for assessing bilirubin levels
HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • Phototherapy – nude under light source, repositioned frequently to expose all body surface areas to light • Frequent bilirubin determination – every 6-12hrs (visual assessment is no longer considered valid)
HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • PHOTOTHERAPY: • PRECAUTIONS: • Eye Shield – opaque mask to prevent exposure to light • Properly sized, correctly positioned without occluding the nares • Infant’s eyelids are closed before mask is applied, corneas may become excoriated • Eyes checked every shift for discharge, excessive pressure on lids, corneal irritation • Removed during feedings • Infants in open crib must have a protective plexiglass shield between them & fluorescent lights to minimize amount of undesirable UV lights reaching skin & protect them from accidental bulb breakage • Temperature monitored • Maintain in flexed position w/ rolled blankets alongside body
HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • PHOTOTHERAPY: • ACCURATE CHARTING: • Times that phototherapy is started and stopped • Proper shielding of the eyes • Type of fluorescent lamp • Number of lamps • Distance between surface of lamps & infant (not <18 in) • Use of phototherapy in combination with an incubator or open bassinet • Photometer measurement of light intensity • Occurrence of side effects • Side effects: loose greenish stools transient skin rashes, hypothermia, Increase BMR, DHN, electrolyte imbalance (hypocalcemia), priapism
HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • PHOTOTHERAPY: • Informed consent prior to treatment • Oily lubricants/lotions not used – “frying effect” • Full-term newborn – additional fluid volume to compensate for fluid loss • Meticulous skin care • Rebound effect – after phototherapy is permanently discontinued  subsequent increase in serum bilirubin level; transient • “Bronze Baby Syndrome” – serum, urine, skin turn grayish brown hours after infant is placed under light • Due to retention of bilirubin breakdown product of phototherapy (copper prophyrin) • Infants with elevated B2 level & some degree of cholestasis • Resolves after discontinuation of phototherapy
RESPIRATORY DISTRESS SYNDROME (RDS) • Condition of surfactant deficiency & physiologic immaturity of thorax • Seen almost exclusively in preterm infants; seen in infants <32 wks AOG • A disease related to developmental delay in lung maturation • Also associated with multifetal pregnancies, infants of diabetic mothers, Caesarean Section delivery, delivery before 37 weeks AOG, low birth weight, precipitous delivery, cold stress, asphyxia, history of previous RDS • Rare in drug-exposed infants or those who have been exposed to chronic intrauterine stress (HPN, preeclampsia) • RDS of nonpulmonary origin in Newborn: sepsis, cardiac defects, exposure to cold, airway obstruction, IVH, hypoglycemia, metabolic acidosis, acute blood loss, drugs.
RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY Deficient Surfactant Collapse of Alveoli Great deal of effort to reexpand the alveoli with each breath Exhaustion Fewer and fewer alveoli opens Atelectasis Hypoperfusion to the lung tissue Hypoxemia and hypercapnia
RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Preterm – born before lungs are fully prepared for gas exchange (critical factor in RDS) • Combination of structural and functional immaturity of lungs • (+) fetal respiratory activity before birth: lungs have feeble respiratory movements, fluid excreted thru alveoli
RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Final unfolding of alveolar septa (increase surface area of the lungs) occurs on last trimester of pregnancy Preterms are born with underdeveloped and uninflatable alveoli Limited pulmonary blood flow Collapsed lungs Increased pulmonary vascular resistance Fetal blood shunted from lungs by ductus arteriosus and foramen ovale
RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Rib Cage: weak and compliant • Fetal chest highly compliant because of predominance of cartilage; diaphragm is prone to fatigue • Fetal Lungs deficient in surfactant due to immaturity of surfactant producing type 2 alveolar cells • Surfactant – 1st produced at 24 wks AOG, type 2 cells do not fully mature until about 36 wks AOG • Reduces surface tension of fluids that line the alveoli & respiratory passages  uniform expansion and maintains lung expansion
RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Deficient surfactant – unequal inflation of alveoli on inspiration, collapse of alveoli of end expiration • Without surfactant – infants unable to keep lungs inflated, exerts great effort to reexpand the alveoli  exhaustion  atelectasis
RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY Inadequate pulmonary perfusion and ventilation Hypoxemia and hypercapnia Markedly reactive pulmonary arterioles and thick Muscular layer decreased oxygen concentration Decreased oxygen tension + decreased blood pH Vasospasm in pulmonary arterioles Increased PVR Intrapulmonary shunting Anaerobic glycolysis Metabolic acidosis, cyanosis
RESPIRATORY DISTRESS SYNDROME (RDS) MAJOR FACTORS IN RDS CAUSE EFFECT Increased surface tension of alveoli (surfactant deficiency) Alveolar collapse, atelectasis, increased difficulty in breathing Impaired gas exchange Hypoxemia, and hypercapnia with respiratory acidosis Increased pulmonary vascular resistance Hypoperfusion of pulmonary circulation Hypoperfusion (with hypoxemia) Tissue hypoxia & metabolic acidosis Increased transudation of fluid into lungs Hyaline membrane formation; impaired gas exchange • PATHOPHYSIOLOGY • (+) pulmonary edema – impaired gas exchange • (+) pulmonary interstitial emphysema – overdistention of distal airways
RESPIRATORY DISTRESS SYNDROME (RDS) • CLINICAL MANIFESTATIONS: • Respiratory Signs and Symptoms: • Tachypnea (80-120/min) initially : dyspnea • Pronounced intercostals and/or substernal retractions • Fine inspiratory crackles ; audible expiratory grunt • Flaring of external nares • Cyanosis / pallor • As disease progresses • Apnea ; flaccidity ; absent spontaneous movement • Unresponsive ; diminished breath sounds ; mottling • Severe disease: shock-like state • Decreased cardiac output and bradycardia • Low systemic BP
RESPIRATORY DISTRESS SYNDROME (RDS) • EVALUATION: • Blood glucose test • Chest x-ray with fine, diffuse, recticogranular or “ground glass appearance and air bronchogram • Arterial blood gas (ABGs) ; pulse oximetry and carbon dioxide monitoring, pulmonary function tests
RESPIRATORY DISTRESS SYNDROME (RDS) • EVALUATION: • Prenatal diagnosis: • Problems like maternal diabetes – delay fetal lung maturation • Antenatal administration of glucocorticoids – enhance fetal lung maturation • Lecithin / sphingomyelin ratio (L:S ratio) : relationship between these 2 lipids during gestation • L:S = 2:1 • “Shake/ bubble test” – stable foam bubbles form when amniotic fluid is shaken in presence of ethanol • Tap Test – abundant bubbles appear in test tube of amniotic fluid with 6N – HCL and diethyl ether • TDx fetal lung maturity assay
RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • Immediate establishment of adequate oxygen and ventilation and supportive measures required for a preterm, prevent further complications • SUPPORTIVE MEASURES: • Maintain adequate ventilation and oxygen • Maintain acid-base balance • Maintain neutral thermal environment • Maintain adequate tissue perfusion and oxygen • Prevent hypotension • Maintain adequate hydration and electrolyte status • NUTRITION: parenteral therapy during 1st phase of disease • Nipple and gavage feedings are contraindicated – causes increase RR, prone to aspiration • Enteral substrate to infant with transient hypoxia – increase risk Necrotizing Enterocolitis
RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • EXOGENOUS SURFACTANT REPLACEMENT (via ET Tube) • Decrease oxygen requirements and mean airway pressure (MAP) • Improves blood gas values & ventilator settings • Decrease incidence of pulmonary air leaks • Decrease deaths from RDS • Decrease mortality rate • COMPLICATIONS: pulmonary hemorrhage, mucous plugging • Given at birth via endotracheal (ET) tube directly into infants trachea • NURSING RESPONSIBILITIES: • Assist in delivery of the product, collection, and monitoring of ABG’s, scrupulous monitoring of oxygen with pulse oximetry • Assess infant’s tolerance of procedure • Delay suctioning for an hour or so to allow maximum effects to occur
RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • OXYGEN THERAPY • Aggressive respiratory support: Oxygen, continuous positive airway pressure (CPAP), intubation, mechanical ventilation • Goals of Oxygen therapy: provide adequate oxygen to tissues • Prevent lactic acidosis resulting from hypoxia • Avoid negative effects of oxygen barotrauma / toxicity • Gas should be warmed before entering respiratory tract • Oxygen can be supplied via plastic hood • If oxygen saturation of blood cannot be maintained at satisfactory level and PaO2 rises  ventilatory assistance
RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED CONVENTIONAL METHODS Continuous Positive Airway Pressure (CPAP) Provides contrast distending pressure to airway in spontaneously breathing infant. Nasal prongs, endotracheal tube, face mask, nasal cannula Positive End-Expiratory Pressure (PEEP) Provides increase end-expiratory pressure during expiration and between Mandatory breaths which prevents alveolar collapse; maintains residual airway pressure Endotracheal intubation, and either volume-limited or pressure-limited ventilator • TREATMENT / MANAGEMENT:
RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED Intermittent Mandatory Ventilation (IMV) Allows infant to breath spontaneously at own rate but provides mechanical cycled respirations and pressure at regular preset intervals Endotracheal intubation and ventilator Synchronized Intermittent Mandatory Ventilation (SIMV) Mechanically delivered breaths are synchronized to the onset of spontaneous patient breaths; assist/control mode facilities full inspiratory synchrony; involves signal detection of onset of spontaneous respiration from abdominal movement, thoracic impedance, airway pressure, or flow changes Patient-triggered infant ventilator with signal detector and assist/control mode; endotracheal tube • TREATMENT / MANAGEMENT:
RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED Volume Guarantee Ventilation Delivers predetermined volume of gas using an inspiratory pressure that varies according to infant’s lung compliance (often used in conjunction with SIMV) Volume guarantee ventilator with flow sensor; endotracheal tube ALTERNATIVE METHODS High frequency Oscillation (HFO) Application of high-frequency, low- volume, sine wave flow oscillations to airway at rates between 480 and 1200 breaths/min Variable-speed piston pump (or loudspeaker, fluidic oscillator) ; endotracheal tube • TREATMENT / MANAGEMENT:
RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED High-Frequency Jet Ventilation (HFJV) Uses separate, parallel, low compliant circuit and injector port to deliver small pulses or jets of fresh gas deep into airway at rates between 250 and 900 breaths/min May be used alone or with low-rate IMV; endotracheal tube • TREATMENT / MANAGEMENT:
RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • COMPLICATIONS OF POSITIVE PRESSURE VENTILATION: • Increased incidence of air leaks that produce complications: • Pulmonary Interstitial Emphysema • Pneumothorax • Pneumomediastinum • Associated with Intubation: • Nasal/tracheal/pharyngeal perforation • Stenosis; inflammation • Palatal grooves; subglottic stenosis • Tube obstruction and infection
RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • INHALED NITRIC OXIDE (NO): for newborn with conditions that cause persistent pulmonary HPN, pulmonary vasoconstriction, subsequent acidosis, and severe hypoxia • Colorless, highly diffusible gas: cause smooth muscle relaxation and reduce pulmonary vasoconstriction and subsequent pulmonary HPN when inhaled into lungs • Administered through ventilator circuit and blended with oxygen • Attaches readily to hemoglobin and deactivated so that systemic vasculature is not affected • Toxic in large quantities • Mucus may collect I respiratory tract as a result of infant’s pulmonary condition  interferes with gas flow and obstruct passages • Catheter inserted gently but quickly; intermittent suctioning (limited to <5secs) • FiO2 increased by 10% before suctioning
RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • Most advantageous position for facilitating an infant’s open airway are on the side with head supported in alignment by small folded blanket • Back position – keep neck slightly extended • Head in “sniffing” position • Inspection of skin – position changes and use of water pillows (prevents skin breakdown) • Mouth care
RESPIRATORY DISTRESS SYNDROME (RDS) • TRANSIENT TACHYPNEA OF THE NEWBORN (RDS TYPE 2) • Delayed resorption of fetal lung fluid; decrease lung compliance • Management: Oxygen therapy • Signs and symptoms similar to RDS 1 (hyaline membrane disease) but resolves 48-72 hrs.
SEPSIS / SEPTICEMIA • Generalized bacterial infection in the bloodstream • Newborns are highly susceptible to infection as a result of diminished nonspecific (inflammatory) & specific (humoral) immunity: impaired phagocytosis, delayed chemotactic response, minimal/absent IgA & IgM, decreased complement levels • High-Risk Infant 4x greater chance; males > females
SEPSIS / SEPTICEMIA • RISK FACTORS: • Prematurity • Congenital Anomalies • Acquired injuries that disrupt the skin, mucous membranes • Invasive procedures – IV lines, ET tubes • Administration of TPNs • Nosocomial exposures – NICU • Infant born after a difficult or traumatic labor & delivery
SEPSIS / SEPTICEMIA • PATHOPHYSIOLOGY: • Premature withdrawal of placental barrier – leaves infants vulnerable to viral, fungal, bacterial, parasitic infections • Early birth interrupts transplacental transmission of passive immunity (IgG) • Preterms – low IgG; IgA & IgM not transferred to fetus
SEPSIS / SEPTICEMIA • SOURCES OF INFECTION: • Acquired prenatally across placenta from maternal blood stream or during labor from ingestion or aspiration of infected amniotic fluid • Prolonged rupture of membranes – maternal-fetal transfer of pathogenic organisms • Transplacental transfer of CMV, toxoplasmosis, syphilis can occur
SEPSIS / SEPTICEMIA • SOURCES OF INFECTION: • Early Sepsis (< 3days) – acquired in perinatal period • Direct contact with organisms from maternal GIT & GUT • Group B streptococcus (GBS), E. Coli • H. influenza, coagulase-negative staphylococci – Very Low Birth Weight infants • Gonococci, Candida albicans, Herpes Simplex Virus II, Listeria organism, Chlamydia • Late Sepsis (1-3 weeks after birth) – nosocomial • Staphylococci, Kleibsiella, enterococci, Pseudomonas • Coagulase-negative staphylococci – Extremely Low Birth Weight, Very Low Birth Weight Infants
SEPSIS / SEPTICEMIA • SOURCES OF INFECTION: • Bacterial Invasion: umbilical stump, mucous membranes of the eyes, nose, pharynx, ear; internal systems (respiratory, nervous, urinary, GIT) • Postnatal Infection: cross-contamination from other infants, personnel, object in the environment
SEPSIS / SEPTICEMIA • SIGNS AND SYMPTOMS: • Systemic Infections – subtle, vague, nonspecific • General: Fever, Temperature instability; “not doing well”; poor feeding, edema • GI System: poor feeding, abdominal distention; vomiting; diarrhea/ decreased stooling; Hepatomegaly, hemoccult-positive stools • Respiratory System: irregular respirations, Apnea/tachypnea; dyspnea, retractions; flaring, grunting; cyanosis • Renal System: Oliguria
SEPSIS / SEPTICEMIA • SIGNS AND SYMPTOMS: • Cardiovascular System/ Circulatory: Pallor/ cyanosis/ mottling, cold clammy skin; hypotension; irregular heartbeat : Tachycardia/ Bradycardia, edema • CNS: diminished activity – lethargy, hyporeflexia, coma • Increased activity – irritability, tremors, seizures • Full fontanelle, High-pitched cry, increased/ decreased tone, abnormal eye movements • Hematologic System: Jaundice, splenomegaly, pallor, petechiae, purpura, ecchymosis
SEPSIS / SEPTICEMIA • DIAGNOSIS: • Based on suspicion of presenting clinical signs and symptoms • Laboratory and radiographic examination – definitive diagnosis • Blood/ urine/ CSF cultures – 10% will have negative cultures • CBC: anemia, leukocytosis/ leucopenia • Leucopenia – ominous sign • C-reactive protein serial measurements • Chest x-ray • Lumbar puncture if < 28 days old, and if with altered mental status or meningeal signs
SEPSIS / SEPTICEMIA • THERAPEUTIC MANAGEMENT: • SUPPORTIVE THERAPY: Circulatory, respiratory • Respiratory distress/ hypoxia : Oxygen therapy • IVF regulation • Correct electrolytes and acid-base balance • NPO temporarily • Blood transfusions for anemia and shock • Vital signs, thermoregulation • Aggressive administration of antibiotics, immunotherapy • Antibiotics X7-10 days if cultures are positive, discontinue in 3 days if culture is negative & infant is asymptomatic (thru IV infusion) • Antifungal/ antiviral therapies
SEPSIS / SEPTICEMIA • PROGNOSIS • Variable • ELBW/ VLBW infants: Early onset sepsis  severe neurologic & respiratory sequelae • Late-onset sepsis & meningitis: poor outcome
SEPSIS / SEPTICEMIA • NURSING CONSIDERATIONS: • Recognize existing problem: “something is wrong” • Awareness of potential modes of infection transmission • Knowledge of the side effects of specific antibiotic & proper regulation & administration of drug are vital • Prolonged antibiotic therapy – (+) growth of resistant organisms & superinfection from fungal/ mycotic agents (Candida albicans) • Nystatin oral suspension swabbed on oral mucosa – prophylaxis • Avoid fully flexed position for obtaining spinal fluid.
SEPSIS / SEPTICEMIA • NURSING CONSIDERATIONS: • Continual cardiorespiratory & pulse oximetry monitoring provides an ongoing assessment of infant’s condition • Decrease additional physiologic or environmental stress • Thermoregulated environment • Anticipate potential problems – dehydration, hypoxia • Precautionary measures: proper hand washing, use disposable equipment • Proper disposal of excretions (vomitus, stool) • Adequate housekeeping • Observe for signs of complications – meningitis, septic shock
NECROTIZING ENTEROCOLITIS • Acute inflammatory disease of the bowel • Seen primarily in premature infants, although, described in full-term neonates as well • Occurs several weeks after birth • ETIOLOGY: • Precise Cause: unknown • Prematurity: risk factor
NECROTIZING ENTEROCOLITIS • ETIOLOGY: • 3 FACTORS THAT PLAY ROLE IN DEVELOPMENT OF NEC: • Intestinal Ischemia – vascular compromise on GIT Diminished Blood Supply Cell death No secretion of protective, lubricating mucus Thin unprotected wall attacked by proteolytic enzyme Bowel wall swell and break down Unable to synthesize IgM, mucosa permeable to toxins Gas-forming bacteria invasion (+) pneumatosis intestinalis (air in submucosa / subserosa)
NECROTIZING ENTEROCOLITIS • ETIOLOGY: • 3 FACTORS THAT PLAY ROLE IN DEVELOPMENT OF NEC: • Colonization by pathogenic bacteria • Substrate (formula feeding) in intestinal lumen – stress on ischemic bowel • SIGNS AND SYMPTOMS: • Nonspecific Clinical Signs: • Lethargy, poor feeding, hypotension • Vomiting, oliguria, hypotension • Unstable temperature, jaundice
NECROTIZING ENTEROCOLITIS • SIGNS AND SYMPTOMS: • Specific Signs: • Distended (often shiny) abdomen; blood in stools/gastric content • Gastric retention; bilious vomitus • Localized abdominal wall erythema/ induration • DIAGNOSIS: • Abdominal x-ray: Sausage-shaped dilation of intestine  distended loops of bowel; “pneumatosis intestinalis” --- “soapsuds” or bubbly appearance of thickened bowel wall & ultralumina; • Air in portal vein; free air under the diaphragm (perforation)
NECROTIZING ENTEROCOLITIS • DIAGNOSIS: • Occult blood in the stool • Blood culture – bacteremia / septicemia • CBC: anemia, leucopenia/ leukocytosis • Metabolic acidosis, electrolyte imbalance • TREATMENT: • Begins with prevention • NPO x 24-48 hours – infants who have suffered birth asphyxia, ELBW, VLBW infants • Breast milk • Minimal enteral feedings – trophic feeding, GIT priming
NECROTIZING ENTEROCOLITIS • TREATMENT: • Confirmed NEC: • Discontinue all oral feedings • Place NGT – for decompression • IV fluids; IV antibiotics • Surgery in extreme cases • PROGNOSIS: • Sequelae of surgical intervention: shirt-gut syndrome, colonic stricture with obstruction, fat malabsorption, failure to thrive
NECROTIZING ENTEROCOLITIS • NURSING CONSIDERATIONS: • Prompt recognition of early warning signs of NEC: abdominal distention, absent bowel sounds • Measure abdominal girth, residual gastric contents before feedings, listen for presence of bowel sounds • Vital signs including blood pressure • Avoid rectal temperatures (danger of perforation) • Avoid pressure on distended abdomen • Infants are left undiapered & positioned supine or on the side • Conscientious attention to nutritional and hydration needs, administration of antibiotics • Oral feedings: started 7-10 days after diagnosis & treatment using human milk, elemental formula • Sterile water may be given initially • Strict hand washing
FAILURE TO THRIVE • Sign of inadequate growth resulting from inability to obtain or use calories required for growth • No universal definition • Common parameter: WEIGHT, sometimes height that falls below 5th percentile for child’s age • Weight for age (height) z value of less than -2.0 • Weight curve (loss) that crosses >2 percentile lines on National Center for Health Statistics (NCHS) growth after previous achievement of a stable growth pattern.
FAILURE TO THRIVE • 3 GENERAL CATEGORIES: • Organic Failure to Thrive • Physical Cause • Congenital heart defects, neurologic lesions, cerebral palsy, microcephaly • Chronic renal failure, gastroesophageal reflux • Malabsorption syndrome, endocrine dysfunction • Cystic fibrosis, acquired immunodeficiency syndrome (AIDS) • Nonorganic Failure to Thrive (NFTT) • Unrelated to disease • Result of psychosocial factors – inadequate nutritional information by parent • Deficiency of maternal care of disturbance in maternal-child attachment • Disturbance in child’s ability to separate from parent leading to food refusal to maintain attention • Idiopathic Failure to Thrive – unexplained by usual organic and environmental etiologies but may also be classified as NFTT.
FAILURE TO THRIVE • Some experts suggest that classifications are too simplistic because most cases of growth failure have mixed causes. • FTT be classified according to pathophysiology for the following categories: • Inadequate Caloric Intake • Incorrect formula preparations • Neglect, food fads • Excessive juice consumption • Poverty • Behavioral problems affecting eating • CNS problems affecting intake
FAILURE TO THRIVE • Inadequate absorption • Cystic fibrosis, celiac disease, vitamin/ mineral deficiencies, biliary atresia, hepatic disease • Increase metabolism • Hyperthyroidism, congenital heart defects, chronic immunodeficiency • Defective utilization • Trisomy 21 or 18, congenital infection, metabolic storage diseases
FAILURE TO THRIVE • ETIOLOGY – multifactorial • Infant organic disease • Dysfunctional parenting behaviors • Subtle neurologic/ behavioral problems • Disturbed parent-child interactions • FACTORS LEADING TO INADEQUATE FEEDING OF INFANT • Poverty – dilute formula to extend available supply; no insurance • No primary care practitioner; homelessness
FAILURE TO THRIVE • Health or childbearing beliefs – fad diets, excessive concern with obesity, hypercholesterolemia, nursing caries • Strict use of scheduled feedings • Inappropriate food source; excessive juice intake • Inadequate nutritional knowledge – cultural confusion (immigrant to USA); cognitive impairments • Family Stress – overwhelming involvement with another chronically ill child • Financial, marital, excessive parenting & employment responsibilities • Single parent employed full time, depression, substance abuse, acute grief
FAILURE TO THRIVE • Psychosocial factors – maternal depression, Munchausen syndrome by proxy, child temperament • Feeding resistance – oral tactile hypersensitivity • Infant receiving nonoral nutritional therapy early in life or exclusively fed with feeding tubes • Insufficient breast milk – fatigue, poor release of milk, breast surgery augmentation, lack of maternal confidence / support.
FAILURE TO THRIVE • CLINICAL MANIFESTATIONS: • Growth Failure – 5th percentile in weight only or weight and height • Developmental delays – social, motor, adaptive, language • Apathy • Poor hygiene • Withdrawn behavior • Feeding/ eating disorder: vomiting, anorexia, pica, rumination • No fear of strangers (stage when stranger anxiety is normal) • Avoidance of eye contact • Wide-eyed gaze & continual scan of environment (radar gaze) • Stiff & unyielding or flaccid & unresponsive • Minimal smiling
FAILURE TO THRIVE • DIAGNOSTIC EVALUATION: • Evidence of growth retardation & caloric deprivation • Anthropometric measurements • Onset of FTT is fairly recent: weigh (not height) is below accepted standards (5th percentile) • Long standing FTT: height and weight depressed; chronic malnutrition • Complete health and dietary history --- history of food consumed over 3-5 day period • Child’s activity level, perceived food allergies, dietary restrictions • P.E for evidence of organic causes, developmental assessment • Family assessment – parental height, household organizations & mealtime behaviors & rituals • Rule out organic causes • Lead toxicity, anemia, stool-reducing substance, occult blood, ova, parasites • Alkaline phospatase, zinc levels
FAILURE TO THRIVE • THERAPEUTIC MANAGEMENT: • Directed as reversing the malnutrition & underlying cause • Goal: provide sufficient calories to support “catch up” growth • Treat any coexisting problems • Multidisciplinary team: physician, nurse, dietitian, gastroenterologist, child- life specialist, social worker or mental health professional • Relieve any additional stresses on family – referrals to welfare agencies or supplemental food programs
FAILURE TO THRIVE • THERAPEUTIC MANAGEMENT: • Family therapy • Behavior modification • Hospitalization indications: • Evidence (anthropometric) of severe acute malnutrition • Child abuse / neglect • Significant dehydration • Caretaker substance abuse or psychosis • Outpatient management that does not result in weight gain
FAILURE TO THRIVE • NURSING CONSIDERATIONS: • Accurate assessment of initial weight & height and daily weight & recording of all food intake • Feeding behavior is documented & parent-child interaction during feeding • Feeding checklist • Should be placed in a room with noninfectious children of similar age • Structure feeding environment to encourage eating
FAILURE TO THRIVE • NURSING CONSIDERATIONS: • The child • May exhibit altered behavioral interactions • Display intense interest in inanimate objects (toys) but less in social interactions • Watchful of people at a distance but become distressed as others come closer • Dislike being touched or held & avoid face-to-face contact; when held they protest briefly on being put down& apathetic when left alone • History of difficulty in feeding, vomiting, sleep disturbance, excessive irritability • Crying during feedings, hoarding food in mouth, rumination after feeding, refusing to switch from liquids to solids, aversion behaviors (turning from food, spitting) • Difficult temperament or passive, sleepy, lethargic infant who does not wake up for feedings
FAILURE TO THRIVE • NURSING CONSIDERATIONS: • The parent • Increased risk for altered parent-infant interactions because: • Isolation and social crisis • Inadequate support systems • Poor / absent parenting role models when they were children • Lack of education, physical/ mental health problems • Physical and sexual abuse, depression, drug dependence, immaturity
FAILURE TO THRIVE • NUTRITIONAL MANAGEMENT: • 4 Primary Goals in Nutritional management of FTT: • Correct nutritional deficiencies & achieve ideal weight for height • Increase caloric intake in formula fed infants: supplements like Polycose, medium chain triglycerides may be added slowly – in 2kcal/oz increments q2-3 days to yield up 28-30 kcal/oz • Carbohydrate additives (8 kcal/tsp)
FAILURE TO THRIVE • NUTRITIONAL MANAGEMENT: • Rice cereal & vegetable oil • Multivitamin supplementation – zinc and iron • Breast-fed infants: add 1 tsp of 24 kcal/oz formula to 3 oz breast milk • Toddlers: high caloric milk (PediaSure) • Fruit juices – minimized in infants < 6 months • Extreme cases: tube feedings or IV therapy • Allow for catch up growth • Restore optimum body composition
FAILURE TO THRIVE • NUTRITIONAL MANAGEMENT: • Educate parents/ primary caregivers regarding child’s nutritional requirements & appropriate feeding methods • Step-by-step directions for formula preparations, written schedule of feeding times • Juices should be avoided in children with growth failure until adequate weight gain has been achieved (should not exceed 4oz/day) • Family-system approach
HEMOLYTIC DISEASE OF THE NEWBORN • Erythroblastosis fetalis • Hyperbilirubinemia in 1st 24 hrs of life • Abnormally rapid rate of RBC destruction • Anemia caused by this destruction (+) production of RBCs  increased # cells for hemolysis • Major causes: isoimmunization (primarily Rh) & ABO incompatibility
HEMOLYTIC DISEASE OF THE NEWBORN • Blood Incompatibility • Antigen / Agglutinogens – substance capable of producing an immune response if recognized by the body as foreign • Antigens + Antibodies = agglutination (clumping) • Antibodies in plasma of 1 blood group (except AB group – no antibodies) produce agglutination when mixed with antigens of a different blood group • ABO blood group system – antibodies occur naturally • Rh system - isoimmunization
HEMOLYTIC DISEASE OF THE NEWBORN 1. Rh Incompatibility • The presence of naturally occurring Rh factor determines the blood type. • Rh (+) – presence of antigen • Rh (-) – absence of antigen • No problems occur when Rh blood type are same in both mother and fetus or if mother is Rh (+) and infant is Rh (-). • Mother Rh (-) and Infant Rh (+) : problem
HEMOLYTIC DISEASE OF THE NEWBORN • Isoimmunization – no effect on 1st pregnancy • Initial sensitization to Rh antigens rarely occurs before the onset of labor • With increased risk of fetal blood transferred to maternal circulation during placental separation, maternal antibody production is stimulated. Fetal RBCs (with antigens foreign to mother) Enters maternal circulation Mother produces anti-Rh antibodies
HEMOLYTIC DISEASE OF THE NEWBORN • Factors that increase incidence of transpalcental hemorrhage & subsequent isoimmunization: • Multiple gestation, abruptio placenta, placenta previa, manual removal of placenta, cesarean delivery Subsequent pregnancy with Rh (+) fetus Previously formed maternal antibodies to Rh (+) blood cells enter fetal circulation Attack and destroy fetal RBCs
HEMOLYTIC DISEASE OF THE NEWBORN • Sensitization may occur during 1st pregnancy if woman had previously received an Rh (+) blood transfusion Fetus compensate for hemolysis and anemia Increase rate of erythropoiesis (+) erythroblasts in circulation Erythroblastosis fetalis
HEMOLYTIC DISEASE OF THE NEWBORN • No sensitization: if there’s strong placental barrier which prevents transfer of fetal blood into maternal circulation • 10-15% of sensitized mothers: no hemolytic reaction in Newborn • Some Rh (-) women even though exposed to Rh (+) fetal blood are unable to produce antibodies to foreign antigen • Most severe form: hydrops fetalis • Fetal hypoxia, cardiac failure, anasarca, effusions (pleural, pericardial, peritoneal) • Stillborn or in severe respiratory distress • Early intrauterine detection: ultrasound, fetal blood sampling • Management: fetal blood transfusions
HEMOLYTIC DISEASE OF THE NEWBORN 2. ABO Incompatibility • Major blood group antigens of fetus are different from those of the mother • Major blood groups: A, B, AB, O • Presence / absence of antibodies & antigens determines whether agglutination will occur
HEMOLYTIC DISEASE OF THE NEWBORN ABO RELATIONSHIP OF ANTIGENS / ANTIBODIES & DONOR- RECIPIENT COMPATIBILITY RBC COMPATIBILITY BLOOD GROUP (PHENOTYPE) GENOTYPE RBC ANTIGENS PLASMA ANTIBODIES AS DONOR TO TYPE AS RECIPIENT FROM TYPE A B AB O AA, AO BB, BO AB OO A B A & B NONE B A NONE A & B AB, A AB, B AB AB, A, B, O O, A O, B O, A, B, AB O
HEMOLYTIC DISEASE OF THE NEWBORN Antibodies in plasma of 1 blood group (except type AB) + Antigens of a different blood group = agglutination (clumping) hemolysis Release large amounts of bilirubin into circulation
HEMOLYTIC DISEASE OF THE NEWBORN • Most common: mother – type O and infant – type A or B • May occur in 1st pregnancy and subsequent pregnancy. Naturally occurring anti-A or anti-B antibodies Present in maternal circulation cross placenta Attack fetal RBC Hemolysis (less severe than Rh incompatibility)
HEMOLYTIC DISEASE OF THE NEWBORN MATERNAL BLOOD GROUP INCOMPATIBLE FETAL BLOOD BROUP O B A A or B A or AB B or AB POTENTIAL MATERNAL-FETAL ABO INCOMPATIBILITIES
HEMOLYTIC DISEASE OF THE NEWBORN • CLINICAL MANIFESTATIONS: • Anemia (hemolysis of RBCs)  jaundice on 1st 24 hours; serum bilirubin elevated (result from liver’s inability to conjugate & excrete excess bilirubin) • Hepatosplenomegaly, varying degrees of hydrops, sign of hypovolemic shock • Hypoglycemia – due to pancreatic cell hyperplasia • DIAGNOSTIC EVALUATION: • Genetic testing • Chorionic Villus Sampling – determine fetal group and type  can lead to abortion • Amniocentesis – fetal blood type  can lead to infection or leaking • Ultrasonography – allow early treatment; used to check amniotic fluid and condition of the placenta • Indirect Coombs Test – evaluate rising anti Rh antibody titers in maternal circulation; done Rh (-) mothers; 1st prenatal visit • Direct Coombs Test – detect antibodies attached to the circulating erythrocytes of affected infants ; done to baby; to determine how extensive is the hemolysis
HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Postnatal therapy: phototherapy for mild cases, exchange transfusion for severe cases • Prevention of Rh isoimmunization: Rho immune globulin (Rhogam) • Human gamma globulin concentrate of anti-D to all unsensitized Rh (-) mothers after delivery or abortion of an Rh-positive infant or fetus • Destroys (by phagocytosis & agglutination) fetal RBCs passing into maternal circulation before they can be recognized by mother’s immune system  immune response is blocked, anti-D antibodies & memory cells not formed
HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Must be administered to unsensitized mothers within 72 hours (possibly as long as 3-4 weeks) after the 1st delivery or abortion & repeated after subsequent ones • Administration of RhIg at 26-28 weeks AOG reduces risk of Rh isoimmunization • Administered thru IM to Rh (-) sensitized women, never to newborn or father • Intravenous immunoglobulin (IVIG) – decreased severity of RBC destruction (hemolysis) in HDN & subsequent development of jaundice • Attacks maternal cells that destroy neonatal RBCs, slows down the progression of bilirubin production • Used in conjunction with phototherapy; decreased necessity for exchange transfusion
HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Intrauterine transfusion – infuse blood into umbilical vein of fetus • Infuse Rh O-negative packed RBCs to raise fetal hematocrit to 40-50% every 2 weeks until fetus reaches 37-38 weeks • Exchange transfusion – infant’s blood removed in small amounts (5-10ml at a time) & replaced with compatible blood (Rh – negative blood) • Removes sensitized RBCs, lowers serum bilirubin, corrects anemia, prevents cardiac failure • Indications: • Rapidly increasing bilirubin level, hemolysis despite intensive phototherapy • Infant born with hydrops fetalis or sign or cardiac failure
HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Fresh whole blood typed & crossmatched to mother’s serum • Amount of donor blood is double the blood volume of infant (85ml/kgBW) but not >500ml • Sterile surgical procedure: catheter  umbilical vein  inferior vena cava • 5-10 ml withdrawn within 15-20 secs  same volume x 60-90 secs
HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • ABO INCOMPATIBILITY • Early detection & implementation of phototherapy • (+) jaundice within 1st 24 hours, increased serum bilirubin levels, RBC spherocytosis, increased ESR: diagnostic of ABO incompatibility • IVIG + phototherapy • Exchange transfusion – not commonly required except when phototherapy fails to decrease bilirubin concentration
HEMOLYTIC DISEASE OF THE NEWBORN • PROGNOSIS: • Severe anemia: result in stillbirth, shock, congestive heart failure, pulmonary/ cerebral complications (cerebral palsy) • With early detection & intrauterine treatment – erythroblastic Newborn rare, exchange transfusions for the conditions less common
HEMOLYTIC DISEASE OF THE NEWBORN • NURSING CONSIDERATIONS: • Initial nursing responsibility – recognizing jaundice • Thru prenatal & perinatal history • Exchange transfusion: prepare infant and family assist practitioner with procedure • Document blood volume exchanged: amount of blood volume withdrawn & infused, time of each procedure, cumulative record of total volume exchanged • Vital signs monitored • (+) signs of cardiac/ respiratory problems: procedure stopped temporarily & resumed once stable • Observe for transfusion reaction
HEMOLYTIC DISEASE OF THE NEWBORN • NURSING CONSIDERATIONS: • Attention on thermoregulation • Hypothermia – increase oxygen and glucose consumption  metabolic acidosis; (-) binding capacity of albumin & bilirubin & hepatic enzyme reaction  kernicterus • Hyperthermia – damages donor’s RBC, increase free K+, predisposes infant to cardiac arrest • Performed with infant under radiant warmer, with sterile drapes, blood is warmed • After procedure: nurse inspects umbilical vein (for bleeding), catheter may remain in place
SUDDEN INFANT DEATH SYNDROME (SIDS) • Sudden death of infant < 1 years old • Unexplained after a complete mortem examination, including an investigation of death scene & review of case history • 3rd leading cause of death in children between 1 month – 1 year ; increased incidence in winter • Incidence: 0.65:1000 live births (1999); males > females • Peak age: 2-4 months; 95% occur by 6 months • Time of death: during sleep • Racial: Native Americans, African Americans, Hispanics • Lower socioeconomic class
SUDDEN INFANT DEATH SYNDROME (SIDS) • Risks: Preterm especially low birth weight; multiple births (2nd twin, male twin & small-for-date twin) • Newborn with low APGAR score • Infants with CNS disturbances & respiratory disorder (bronchopulmonary dysplasia/ chronic lung disease) • Increased birth order (subsequent siblings as opposed to 1st born child) • Infants with recent history of mild illness
SUDDEN INFANT DEATH SYNDROME (SIDS) • Sleep in prone position • Cause oropharyngeal obstruction or affect thermal balance or arousal state • Rebreathing of carbon dioxide by prone infant & impaired arousal from active & quiet sleep • Side-lying position no longer recommended – tends to turn to prone position • Use of soft bedding – not able to move their heads to the side  suffocation and lethal rebreathing • Overheating (thermal stress); co-sleeping with adult especially on sofa • Adult beds/ sofas are not designed for infants & may carry risk of accidental entrapment & suffocation
SUDDEN INFANT DEATH SYNDROME (SIDS) • Lower incidence in breast-fed infants – pacifier may be protective against SIDS • Maternal risk: young age, cigarette smoking especially during pregnancy • Poor prenatal care, substance abuse (heroin, methadone, cocaine) • 12% of all SIDS death could be prevented with prenatal smoking cessation • Maternal smoking decreases infant’s ability to arouse to auditory stimuli in mothers who smoke prenatally.
SUDDEN INFANT DEATH SYNDROME (SIDS) • ETIOLOGY: • Unknown • Hypothesis: related to brainstem abnormality in neurologic regulation of cardiorespiratory control • Abnormalities: prolonged sleep apnea, increased frequency of brief inspiratory pauses, excessive periodic breathing, impaired arousal responsiveness to increase carbon dioxide or decrease oxygen • Sleep apnea is not the cause of SIDS; genetic predisposition has been postulated as the cause • Autopsies: pulmonary edema & intrathoracic hemorrhages • Should be performed on all infants suspected of dying of SIDS
SUDDEN INFANT DEATH SYNDROME (SIDS) • INFANTS AT RISK FOR SIDS: • Infants with 1 or more ALTEs requiring cardiopulmonary resuscitation (CPR) or vigorous stimulation • Preterm infants who continue to have apnea at the time of hospital discharge • Siblings of 2 or more SIDS victim • Infants with certain types of disease or conditions – central hypoventilation • Home monitoring and/or use of respiratory stimulant drugs recommended • No diagnostic tests exist to predict which infants will survive
SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Educate families in prevention of SIDS • Risk of prone sleeping position in infant births – 6 months • Use of appropriate beddings, parental smoking around infant and dangers of sharing an adult bed with infant • Post partum discharge planning, newborn discharge teaching and newborn- care classes • Follow-up visits, well-baby clinic visits, immunization visits • Discuss infant sleep position
SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Psychologic intervention – loss of child • Practices that may reduce the risk of SIDS • Avoid smoking during pregnancy and near the infant • Encouraging supine sleeping position • “back to sleep” • Avoid soft, moldable mattresses, blankets, pillows • No pillows/ quilts, stuffed toys, towels • Discouraging bed sharing • Encourage breastfeeding
SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Avoid overheating during sleep • Infants should wear light-clothing, comfortable room temperature • Infant’s head position should be varied to prevent flattening of the skull • Use of pacifier – protective against occurrence of SIDS; naptime and bedtime, no sweetened coating • Finding the infant • it’s always the mother who finds child dead in crib • Child is in disheveled bed w/ blankets over head, huddled in 1 corner
SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Frothy, blood-tinged fluid fills the mouth & nostrils, lying face down in secretions (bled to death) • Diaper is wet and full of stool – cataclysmic type of death • Parents must deal with his/her initial shock, panic, grief • Compassionate, sensitive approach to family
SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Arriving at emergency department • No attempt at resuscitation • Parents are asked only factual questions – when they found the infant, how he/she looked • No misguided statements: “this looks like suffocation” (guilt) • Discuss possible autopsy • Compassionate care – allow them to say good-bye to their child
APNEA OF PREMATURITY (AOP) • Preterm infants; rare: full-term • Apneic spells increase in prevalence the younger the gestational age • 1/3 infants <33 weeks AOG, >1/2 healthy infants < 30 weeks AOG • Resolves as infant reaches 37 weeks postmenstrual age • Preterms are periodic breathers – periods of rapid respirations separated by periods of very slow breathing, often short periods with no visible or audible respirations • Apnea – extension of periodic breathing • Lapse of spontaneous breathing for 20 seconds or longer, that may or may not be followed by bradycardia, oxygen desaturation and color change • Temporary apnea - <15-20 seconds • Pathologic apnea - > 20 seconds
APNEA OF PREMATURITY (AOP) • Classification according to origin: • Central Apnea – absence of diaphragmatic and other respiratory effort • Occurs when CNS does not transmit signals to the respiratory muscle • Obstructive Apnea – air flow ceases because of upper airway obstruction yet chest or abdominal wall movement is present • Mixed Apnea: combination of central and obstructive apnea • Most common apnea seen in preterm infants
APNEA OF PREMATURITY (AOP) • PATHOPHYSIOLOGY: • Reflects the immature and poorly refined neurologic and chemical respiratory control mechanism in premature infants • Not responsive to hypercarbia and hypoxemia, have fewer dendritic associations than those of more mature infants • Respiratory reflexes less mature – contributing factor in etiology • Weakness of muscles of thorax, diaphragm and upper airway – contribute to apneic episodes
APNEA OF PREMATURITY (AOP) • PATHOPHYSIOLOGY: • Apnea – observed during periods of REM sleep • Precipitated/ worsened by a variety of factors: • Infection • Intracranial hemorrhage • PDA • Secondary causes: investigated in infants with new-onset apnea or when there’s significant change in frequency or severity of apneic episodes • Apnea in full-term: consider secondary cause
APNEA OF PREMATURITY (AOP) • POSSIBLE CAUSES OF APNEA OF PREMATURITY: • Prematurity • Airway obstruction with mucus or milk, or poor positioning • Anemia, polycythemia • Dehydration • Cooling / overheating • Hypoxemia • Hypercapnia / hypocapnia • Hypoglycemia, hypocalcemia, hyponatremia • Sepsis, meningitis • Seizures • Increased vaga tone (in response to suctioning nasopharynx, gavage tube insertion, reflux of gastric contents, endotracheal intubation) • CNS depression – pharmacologic agents • Intraventricular hemorrhage (IVH) • Patent ductus arteriosus (PDA), congestive heart failure (CHF) • Depression following maternal obstetric sedation • Respiratory distress – pnemonia, inborn errors of metabolism (hyperammonemia), congenital defects of upper airways
APNEA OF PREMATURITY (AOP) • CLINICAL MANIFESTATIONS: • Persistent apneic spells • TREATMENT • Observe for apnea • Check for thermal stability • Administration of methylxanthines (theophylline, aminophylline or caffeine) • Reduce frequency of primary apnea-bradycardia spells in newborn • CNS stimulants to breathing • Observe for symptoms of toxicity • Caffeine – fewer side effects ; once daily dosing • Monitor weight and urine output
APNEA OF PREMATURITY (AOP) • TREATMENT: • Nasal continuous positive airway pressure (NCPAP) and intermittent positive pressure ventilation • CPAP acts to maintain airway patency • More effective for obstructive/ mixed apnea
APNEA OF PREMATURITY (AOP) • NURSING CONSIDERATION: • Monitor respiration and heart rate routinely in all preterm infants • Observe for presence of respirations • Observe color • Provide gentle tactile stimulation – rubbing the back/ chest gently, turning infant to supine position • If tactile stimulation fails to reinstitute respiration – flow by oxygen and suctioning of nose and mouth • Apply artificial ventilation with bag-valve mask and with sufficient pressure to lift rib cage • If breathing does not begin • Raise chin gently to open airway • Infant is never shaken
APNEA OF PREMATURITY (AOP) • NURSING CONSIDERATION: • After breathing is restored: assess for and manage any precipitating factors (temperature instability, abdominal distention, ambient oxygen) – use pulse oximetry • Record episodes of apnea - # apneic spells, appearance during and after the episode, did infant self-recover or whether tactile stimulation or other measures were done to restore breathing. • Investigate possible cause of apneic episode • Observe for signs of theophylline or caffeine toxicity; tachycardia (rate 180-190/ min) and later, vomiting, restlessness, irritability • Assess skin (with NCPAP) for breakdown, irritation, and nasal septum
AUTISTIC SPECTRUM DISORDER (AUTISM) • Complex developmental disorder of brain function accompanied by intellectual and behavioral deficits • Manifested during early childhood: 18-36 months of age • 1-2 in 500 children; males > females (females more severely affected) • Not related to socioeconomic level, race, parenting style
AUTISTIC SPECTRUM DISORDER (AUTISM) • ETIOLOGY • Unknown • Multiple biologic causes • Abnormal EEG, epileptic seizures, delayed development of hand predominance, persistence of primitive reflexes, metabolic abnormalities (increased serotonin), hypoplasia of vermis of cerebellum • Increased in twins • High risk of recurrence of ASD in families with one affected child • Not caused by thimerosal-containing vaccines • Associated with fragile X syndrome, tuberous sclerosis, metabolic disorder, fetal rubella syndrome, H. influenza meningitis, structural brain anomalies • Perinatal events: higher incidence of maternal uterine bleeding during pregnancy • Lower incidence of maternal vaginal infections during pregnancy • Decreased maternal use of contraceptives • Higher incidence of neonatal hyperbilirubinemia
AUTISTIC SPECTRUM DISORDER (AUTISM) • CLINICAL MANIFESTATIONS AND DIAGNOSTIC EVALUATION: • Hallmark: inability to maintain eye contact with another person • Display limited functional play and may interact with toys in an unusual manner • Deficits in social development: primary feature of illness • Majority have some degree of mental retardation • Females tend to have very low intelligence scores • Savants – children with ASD who excel in particular areas: art, music, memory, mathematics, perceptual skills (puzzle building)
AUTISTIC SPECTRUM DISORDER (AUTISM) • Speech and language delays • Immediate evaluation of any child who does not display such language skills as babbling or gesturing by 12 months, single word by 16 months, 2-word phrases by 24 months • Sudden deterioration in extant expressive speech is also a red-flag event for further evaluation
AUTISTIC SPECTRUM DISORDER (AUTISM) • DIAGNOSTIC CRITERIA FOR ASD: • Total of 6 (or more) items from (1), (2), (3) with at least two from (1), and one each from (2) & (3) (1) Qualitative impairment in social interaction, as manifested by at least 2 of the following: • Marked impairment in use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, & gestures to regulate social interaction • Failure to develop peer relationships appropriate to developmental level • A lack of spontaneous seeking to share enjoyment, interests, or achievements w/ other people (ex. By a lack of showing, bringing, or pointing out objects of interest) • Lack of social/ emotional reciprocity
AUTISTIC SPECTRUM DISORDER (AUTISM) (2) Qualitative impairments in communication as manifested by at least 1 of the following: • Delay in, or total lack, of the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime) • In individuals w/ adequate speech, marked impairment in the ability to initiate or sustain a conversation with others • Stereotyped and repetitive use of language or idiosyncratic language • Lack of varied, spontaneous, make-believe play or social imitative play appropriate to developmental level
AUTISTIC SPECTRUM DISORDER (AUTISM) (3) Restricted repetitive and stereotyped patterns of behavior, interests & activities, as manifested by at least 1 of the following: • Encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus • Apparently inflexible adherence to specific, nonfunctional routines or rituals • Stereotyped & repetitive motor mannerisms (ex. Hand or finger flapping or twisting, or complex whole- body movements) • Persistent preoccupation w/ parts of objects • Delays or abnormal functioning in at least 1 of the following areas with onset before age 3 years • Social interaction • Language as used in social communication • Symbolic or imaginative play • The disturbance is not better accounted for by Rett disorder or childhood disintegrative disorder
AUTISTIC SPECTRUM DISORDER (AUTISM) • PROGNOSIS: • Severely disabling condition • Some improve with acquisition of language skills & communication w/ others • Some achieve independence, but most require lifelong adult supervision • Aggravation of psychiatric symptoms – ½ children during adolescence, w/ girls having tendency for continued deterioration • Most favorable for children who develop communicative speech by age, years & have an IQ higher than 50 at time of diagnosis
AUTISTIC SPECTRUM DISORDER (AUTISM) • NURSING CARE MANAGEMENT: • No cure for ASD but there are numerous therapies • Highly structured & intensive behavior modification programs • Promote positive reinforcement, increase social awareness of others, teach verbal communication skills and decrease unacceptable behavior • Provide a structured routine for the child to follow – key management in ASD
AUTISTIC SPECTRUM DISORDER (AUTISM) • NURSING CARE MANAGEMENT: • Hospitalized child with ASD: dcrease stimulation • Place child in private room • Avoid extraneous auditory & visual distraction • Encourage parents to bring in possessions to which child is attached • Minimum holding & eye contact • Care must be taken when performing procedures, administering meds, feeding these children – may swallow thermometer, gags when eating • Family support - counseling
MAJOR STRESSORS OF HOSPITALIZATION • SEPARATION ANXIETY • Middle infancy – preschool age • STAGES: • PROTEST PHASE: • Cry and scream • Cling to parent • Avoids/ rejects contact with strangers • Verbally and physically attack strangers • Attempts to escape and find parents
MAJOR STRESSORS OF HOSPITALIZATION • DESPAIR PHASE: • Crying stops, evidence of depression • Less active • Uninterested in food • Withdraws from others • Child’s physical condition may deteriorate from refusal to eat, drink, or move • DETACHMENT PHASE: • Denial; resignation and not contentment • Child becomes more interested in the surroundings • Forms new but superficial relationship • May have serious attachment to parent after separation
MAJOR STRESSORS OF HOSPITALIZATION • LOSS OF CONTROL • INFANTS • Trust • Consistent, loving caregivers • Attempts to control their environment through emotional expressions • TODDLERS • Autonomy • When their egocentric pleasures meet with obstacles, they react with negativism • Results from altered routines and rituals
MAJOR STRESSORS OF HOSPITALIZATION • PRESCHOOLERS • Suffer loss of control by physical restriction, altered routines, and enforced dependency • Egocentric and magical thinking typical of age • May view illness and hospitalization as punishment for misdeed • PREOPERATIONAL THOUGHT – explanations are understood only in terms of real events • TRANSDUCTIVE REASONING – deduct from the particular to particular, rather than from the specific to the general
MAJOR STRESSORS OF HOSPITALIZATION • SCHOOL AGE • Striving for independence and productivity • Altered family roles, physical disability, fears of death, abandonment, permanent injury, loss of peer acceptance, lack of productivity • Boredom • ADOLESCENTS • Struggle for independence, self assertion and liberation – personal identity • Separation from peer group • May respond with anger, frustration • Voluntarily isolate themselves from age mates until they can feel they can compete • Need for information about their condition
MAJOR STRESSORS OF HOSPITALIZATION • FEARS OF BODILY INJURY AND PAIN • Common fear among children • May persist into adulthood and result in avoidance of needed care • YOUNG INFANT’S RESPONSE TO PAIN: <6 months • Generalized response of rigidity, thrashing • Loud crying • Facial expressions of discomfort – most consistent indicator of stress • No understanding of the relationship between stimuli and subsequent pain.
MAJOR STRESSORS OF HOSPITALIZATION • OLDER INFANT’S RESPONSE TO PAIN: (6months – 1year) • Withdrawal from painful stimuli • Loud crying • Facial grimace • Physical resistance • YOUNG CHILD’S RESPONSE TO PAIN: (toddlers) • Loud crying; screaming • Verbalization, “ow”, “ouch”, “it hurts” • Thrashing of limbs • Attempts to push away stimulus • Uncooperative; needs restraints • Clings to parent, nurse, or other significant person • Request emotional support
MAJOR STRESSORS OF HOSPITALIZATION • SCOOL-AGE CHILD’S RESPONSE TO PAIN • Stalling behavior – “wait a minute”, “I’m not ready” • Muscle rigidity • May use all behaviors of young child • ADOLESCENT’S RESPONSE TO PAIN • Less vocal protest, less motor activity • Increased muscle tension and body control • More verbalization (“It hurts”, You’re hurting me!”)
INDIVIDUAL RISK FACTORS THAT INCREASE VULNERABILITY TO STRESSES OF HOSPITALIZATION • “Difficult” temperament • Lack of fit between child and parent • Age (especially between 6 months and 5 years old) • Male gender • Below average intelligence • Multiple and continuing stresses (ex. Frequent hospitalizations)
BENEFICIAL EFFECT OF HOSPITALIZATION • Recovery from illness • Increase coping skills • Master stress and feel competent in coping • New socialization experiences
PREVENTING OR MINIMIZING SEPARATION • Primary nursing goal • Especially for children < 5 years old • Family-centered care • Parents are not “visitors” • Familiar items from home
NORMALIZING THE HOSPITAL ENVIRONMENT • Maintain child’s routine, if possible • Time structuring • Self-care (age appropriate) • School work • Friends and visitors
PREVENTING OR MINIMIZING FEAR OF BODILY INJURY • All children fear bodily injury from mutation, bodily intrusion, body- image change, disability, or death. • Preparation of children for painful procedures decreases their fears. • Use of bandages • Repeatedly stress the reason for a procedure • Adolescents may express concern about the actual procedure but more anxious about the resulting scar.
PAIN FACTS AND FALLACIES • FACT: Children are under treated for pain. • FACT: Analgesia is withheld for fear of the child becoming addicted • FALLACY: Analgesia should be withheld because it may cause respiratory depression in children • FALLACY: Infants do not feel pain.
PRINCIPLE OF PAIN ASSESSMENT IN CHILDREN: QUESTT • Question the child. • Use pain rating scale. • Evaluate behavioral & physiologic changes. • Secure parent’s involvement. • Take the cause of pain into account. • Take action and evaluate result. • Question the child – verbal & description of pain. Ask child to point where it hurts. • Use of Pain Rating Scale – provide a quantitative self-reporting measure of pain.
PAIN RATING SCALES • Not all pain rating scale are reliable or appropriate for children • Should be age appropriate • Consistent use of same scale by all staff. • Familiarize child with scale
PAIN RATING SCALE F.L.A.C.C (FACE, LEGS, ACTIVITY, CRY, CONSOLABILITY 0 1 2 FACE No particular expression or smile Occasional grimace or frown, withdrawn, disinterested Frequent to constant frown, clenched jaw, quivering chin LEGS ACTIVITY Normal, relaxed position, moves easily Uneasy, restless, tense, shifting back and forth Arched, rigid or jerking CRY No cry (awake or asleep) Moans, whimpers, occasional complaint Crying steadily, screams or sobs, frequent complaints CONSOLABILITY Content, relaxed Reassured by occasional touching, hugging or talking to Difficult to console or comfort
CHILDREN’S DEVELOPMENTAL CONCEPT OF ILLNESS • PREOPERATIONAL THOUGHT (2-7years) • PHENOMENISM – perceives an external, unrelated, concrete phenomenon as cause of illness • CONTAGION – perceives cause of illness as proximity between 2 events that occur by magic
CHILDREN’S DEVELOPMENTAL CONCEPT OF ILLNESS • CONCRETE OPERATIONAL THOUGHT (7-10years) • CONTAMINATION – perceives cause as a person, object, or action external to the child that is “bad” or “harmful” to the body • INTERNALIZATION – perceives illness as having an external cause but as being located inside the body
CHILDREN’S DEVELOPMENTAL CONCEPT OF ILLNESS • FORMAL OPERATIONAL THOUGHT (13yrs & above) • PHYSIOLOGIC – perceives cause as malfunctioning or nonfunctioning organ or process; can explain illness in sequence of events • PSYCHOPHYSIOLOGIC – realizes that psychologic actions and attitudes affect health and illness.

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High risk newborns and child during illness and hospitalization pediatric nursing

  • 1.
  • 2. HIGH RISK NEWBORN • High Risk Neonates  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 extrauterine existence.
  • 3. HIGH RISK NEWBORNS • Encompasses human growth and development from the time of viability – 28 days following birth and includes threat to life and health that occur during the prenatal, perinatal, and postnatal periods. • Viability – gestational age at which survival outside the uterus is believed to be possible, or as early as 23 weeks of gestation.
  • 4. CLASSIFICATION OF HIGH-RISK NEWBORN • Birth Weight • Gestational Age – preterm/post term • Predominant Physiologic Factors – associated with state of maturity; chemical disturbances (hypoglycemia, hypocalcemia); consequences of immature organ systems (hypothermia, Respiratory Distress Syndrome,
  • 5. CLASSIFICATION ACCORDING TO SIZE • Low Birth Weight – less than 2500g regardless of gestational age • Moderately Low Birth Weight – birth weight is between 1501g to 2500g. • Very Low Birth Weight – birth weight is less than 1500g. • Extremely Low Birth Weight – birth weight less than 1000g.
  • 6. CLASSIFICATION ACCORDING TO SIZE • Appropriate for Gestational Age (AGA) – birth weight falls between the 10th and 90th percentile • Small for Gestational Age (SGA) – birth weight falls below the 10th percentile • Large for Gestational Age (LGA) – birth weight falls above the 90th percentile
  • 7. CLASSIFICATION ACCORDING TO GESTATIONAL AGE • Premature Infant – born before the completion of 37 weeks of gestation, regardless of birth weight • Full-Term Infant – born between the beginning of the 38 weeks and the completion of the 42 weeks of gestation • Postmature Infant – born after 42 weeks of gestational age, regardless of birth weight
  • 8.
  • 9. PRETERM INFANTS • An infant born before term (</=36 weeks); premature or preterm • A low birth weight infant: </=1300-2000g (Philippine Standards) (,2.5kg) • Born before complete maturity; born before body and organ system have completely matured. • PRETERM: refers to pregnancy (PT labor); PREMATURE: to describe a baby
  • 10. PRETERM INFANTS INCIDENCE: • Highest among low socio economic class • Largest # of admission to NICU • 12% of all pregnancies • Multiple pregnancies • PIH • Placental problems
  • 11. PRETERM INFANTS CAUSES: • UNKNOWN • MATERNAL FACTOR • Malnutrition • Preeclampsia (toxemia of pregnancy) • Chronic Medial illness (Cardiac/kidney disease/DM) • Infection (UTI, vaginal infection) • Drug Use (coccaine, tobacco, alcohol) • Abnormal structure of the uterus • Previous PT Births
  • 12. PRETERM INFANTS CAUSES: • PREGNANCY • Hypertension • Incompetent Cervix • Placental Previa/ Abruptio Placenta • PP.OM, poly/oligohydramnios • FETUS • Chromosomal abnormalities • Intrauterine Infection • Anatomic Abnormalities • IUGR, multiple gestations
  • 13. PRETERM INFANTS DIAGNOSTIC EVALUATION: • Appraisal is made as soon as possible after admission to the nursery. • HEAD – head circumference is large in comparison with chest (reflects cephalocaudal direction of growth) • The fontanels are small and bones are soft • Soft cranium subject to characteristic nonintentional deformation, “preemie head” • Absent eyebrows, eyes closed, and ears are poorly supported by cartilage (soft and pliable) • Bones of skull and ribs – soft • Very small and appear scrawny – less subcutaneous fat (skin is wrinkled)
  • 14. PRETERM INFANTS DIAGNOSTIC EVALUATION: • SKIN – bright pink (often transluscent) with small blood vessels • Smooth and shiny (may be edematous) with small blood vessels clearly visible underneath thin epidermis • Fine lanugo hair abundant over body, sparse, fine & fuzzy on head • Soles and palms – minimal creases • Harlequin color – Skin color changes when preterm infant is moved; upper half or one side of the body is pale or one side of the body is red. • Small breast bud size with underdeveloped nipples • Male Infants – few scrotal rugae, undescended testes
  • 15. PRETERM INFANTS DIAGNOSTIC EVALUATION: • Labia and clitoris are prominent in females • Posture - complete relaxation with marked flexion and abduction of the thighs; random movements are common with slightest stimulus • Activity – Inactive and listless • Extremities maintain an attitude of extension and remain in any position in which they are placed. • Reflexes – partially developed • Sucking absent, weak or ineffectual; swallow, gag, cough reflexes – ABSENT • Temperature instability – Heat regulation poorly developed in the preterm infant because of poor development of CNS • Increased susceptibility to infection
  • 16. PRETERM INFANTS DIAGNOSTIC EVALUATION: • Respirations are not efficient because of muscular weakness of lungs and rib cage and limited surfactant production; • Retraction at xiphoid is evidence of air hunger • Infants should be stimulated if apnea occurs • HMD/RDS, chronic lung disease, BPD, apnea of prematurity • Greater tendency toward capillary fragility in the preterm infant • Red and white blood cell counts are low with resulting anemia during first few months of life. • Neuro – Higher incidence of intracranial hemorrhage in the preterm infant • Muscle twitching, convulsions, cyanosis, abnormal respirations, and a short shrill cry • Cerebral palsy, visual-motor deficits, altered intellectual functions
  • 17. PRETERM INFANTS DIAGNOSTIC EVALUATION: • GIT: Nutrition is difficult to maintain – because of weak sucking and swallowing reflexes, small capacity of stomach, and slow emptying time of the stomach • Renal: Reduced glomerular filtration rate results in decreased ability to concentrate urine and conserve fluid. • Higher ECF – vulnerable to fluid and electrolyte imbalance • Cardio: (+) murmur • More susceptible to biochemical alterations – hyperbilirubinemia, hypoglycemia • The greater degree of immaturity, the greater the degree of potential disability.
  • 18. PRETERM INFANTS THERAPEUTIC MANAGEMENT: • Team approach: neonatologist, advance practice nurse, nurse staff, respiratory therapist • Incubator, IV lines, Oxygen therapy • PREVENTION: • PRENATAL CARE: key factor • Good nutrition and education • ID mothers at risk • Educate on symptoms of PT labor • Avoid heavy/repetitive work or standing long periods of time
  • 19. PRETERM INFANTS THERAPEUTIC MANAGEMENT: • TREATMENT: • Oxygen, IVF • Umbilical catheterization – IVF, meds, bld extraction • X-ray • Special feedings of breastmilk/formula • Medications • Kangaroo care – shorter stay in NICU
  • 20. PRETERM INFANTS THERAPEUTIC MANAGEMENT: • DISCHARGE: • Usually stay in hospital until reach pregnancy due date depending on their condition • GOALS: • Serious illness resolved • Stable temperature • Taking all feedings by breast/bottle • No recent apnea/bradycardia • Parents are able to provide care (meds and feedings) • Prior to discharge: eye examination, follow up visits
  • 21. PRETERM INFANTS NURSING CARE: • IMPLEMENTATION: • Maintain airway; check respirator function if employed; position to promote ventilation; suction when necessary; maintain temperature of environment; administer oxygen only if necessary • Observe for changes in respirations, color, and vital signs • Check efficacy of Isolette: maintain heat, humidity, and oxygen concentration; monitor oxygen carefully to prevent retrolental fibroplasias • Maintain aseptic technique to prevent infection • Adhere to the techniques of gavages feeding for safety of the infant
  • 22. PRETERM INFANTS NURSING CARE: • IMPLEMENTATION: • Observe weight-gain patterns • Determine blood gases frequently to prevent acidosis • Institute phototherapy by letting them verbalize and ask questions to relieve anxiety • Provide flexible and liberal visiting hours for parents as soon as possible • Allow parents to do as much as possible for the infant after appropriate teaching • Arrange follow-up before and after discharge by a visiting nurse or a Barangay Health Worker
  • 23.
  • 24. POST MATURE INFANTS • After 42 weeks AOG/ 294 days past 1st day of mother’s LMP; regardless of birth weight • Post term, post maturity, prolonged pregnancy, post datism • INCIDENCE: • 7% (3.5-15%) OF ALL PREGNANCIES • CAUSES: unknown • History of >/= 1 previous post term pregnancies & miscalculated due date (not sure of LMP)
  • 25. POST MATURE INFANTS FETAL RISK: • Progressive placental dysfunction – placenta (supplies nutrient & oxygen) ages toward the end of pregnancy --- may not function efficiently • Amniotic fluid volume decreases, fetus may stop gaining weight/ weight loss • Decreased amniotic fluid may lead to cord compression during labor • Increased risk of MAS and hypoglycemia • Increasing size (mainly length) & hardening of skull may contribute to CPD • GREATEST RISK: during stresses of labor & delivery especially in infants of primigravidas.
  • 26. POST MATURE INFANTS CHARACTERISTICS OF INFANTS (1-3wks of AGE): • Absent lanugo, little if any vernix caseosa, abundant scalp hair, overgrown nails • Dry, peeling skin (cracked, parchmentlike & desquamating) • Wasted physical appearance (reflects intrauterine deprivation) • Minimal fat deposit (depleted subcutaneous fat) – thin, elongated appearance • Meconium staining – seen in skin folds w/ vernix caseosa • Visible creases palms/ soles
  • 27. POST MATURE INFANTS DIAGNOSIS: P.E • UTZ, non-stress testing, estimate amniotic fluid volume MANAGEMENT: • Check respiratory problems related to meconium • Blood test for hypoglycemia • PREVENTION: • Accurate due date and UTZ • Cesarean section/ induction of labor - recommended
  • 28.
  • 29. HYPERBILIRUBINEMIA • Refers to excessive level of accumulated Bilirubin in the blood • JAUNDICE or ICTERUS – yellowish discoloration of skin, sclera, nails • Relatively benign but it can also be pathologic
  • 30. HYPERBILIRUBINEMIA PATHOPHYSIOLOGY: RBC DESTRUCTION Globin Heme Unconjugated Bilirubin liver Bilirubin detched from albumin through enzyme glucoronyl transferase + glucoronic acid Conjugated Bilirubin Excreted into Bile (feces and urine) Protein (used by the body)
  • 31. HYPERBILIRUBINEMIA PATHOPHYSIOLOGY: • Result from increased unconjugated/ conjugated bilirubin • Bilirubin – one of the breakdown products of hgb from RBC destruction • Unconjugated Bilirubin – insoluble, bound to albumin • Intestines – (+) bacterial action – reduces conjugated bilirubin • Urobilinogen – pigment that gives stool its characteristic odor.
  • 32. HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE CAUSE: Immature hepatic function + increased bilirubin load from RBC hemolysis Decreased milk intake related to fewer calories consumed by infant before mother’s milk is well established; enterohepatic shunting Possible factors is breast milk that prevent bilirubin conjugation Less frequent stooling Blood antigen incompatibility causes hemolysis of large # of RBCs. Liver unable to conjugate & excrete excess bilirubin from hemolysis COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
  • 33. HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE ONSET: After 24 hours (preterm infants, prolonged) 2nd – 4th day 5th – 7th day During 1st 24 hrs (levels increase faster than 5mg/ml/day) PEAK: 75 – 90 hours 3rd – 5th day 10th – 15th day Variable DURATION: Declines on 5th-7th day Variable May remain jaundiced x 3- 12 weeks or more Dependent on severity & treatment COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
  • 34. HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE THERAPY: Increase frequency of feedings & avoid supplements. Evaluate stooling pattern. Monitor Transcutaneous Bilirubin (TcB)/ Total Serum Bilirubin (TSB) Frequent (10-12x/day) breastfeeding, avoid glucose water, water supplements or formula. Evaluate stooling pattern; stimulate as needed. Increase frequency of breast feeding; use no supplementations (glucose water); cessation of breastfeeding not recommended. Perform risk assessment. Monitor TcB/TSB level. Perform risk assessment POST NATAL – phototherapy; administer IVIG per protocol; if severe, perform exchange transfusion. COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
  • 35. HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE THERAPY: Perform risk assessment. Use phototherapy if bilirubin level increases significantly (>5mg/dl/day) or significant hemolysis is present. Use phototherapy if bilirubin level increases significantly (17-22mg/dl) or significant hemolysis is present. Consider performing additional evaluations: G6PD, direct and indirect serum bilirubin, family history & others as necessary. PRENATAL – transfusion (fetus) Prevent sensitization (Rh Incompatibility) of Rh- negative mother with Rhig (Rhogam) COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
  • 36. HYPERBILIRUBINEMIA BREAST-FEEDING- ASSOCIATED JAUNDICE (EARLY ONSET) BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE THERAPY: If phototherapy is instituted, evaluate benefits & harm of temporarily discontinuing breastfeeding; additional assessments may be required. Assist mother with maintaining milk supply, feed expressed milk as appropriate. After discharge, follow up according to hour of discharge. May include home phototherapy with a temporary (10-12hr) discontinuation of a breastfeeding; a subsequent TSB may be drawn to evaluate a drop in serum levels. Assist mother with maintenance of milk supply & reassurance regarding her milk supply and therapy. Use formula supplements only at practitioner’s discretion. PRENATAL – If mother is breastfeeding, assist with maintenance & storage of milk; may bottle-feed expressed milk as appropriate to therapy. Minimize maternal-infant separation & encourage contact as appropriate. COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
  • 37. HYPERBILIRUBINEMIA POSSIBLE CAUSES: • PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): • Physiologic Jaundice / Icterus Neonatorum – most common cause; no pathologic process 2 PHASES: term infants • 1ST phase – Bilirubin: 6mg/dl on 3rd DOL  decreased to 2-3mg/dl by 5th day • 2nd phase – Steady plateau without increase/decrease level  12th-14th day: levels decresed to normal (1mg/dl) • Pattern varies according to racial group, method of feeding, gestational age PRETERM: Bilirubin – 10-12mg/dl at 4-5days  slowly decrease by 2-4 weeks.
  • 38. HYPERBILIRUBINEMIA POSSIBLE CAUSES: • PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): • Mechanisms Involved: • NB produce 2x as much bilirubin as do adults due to higher concentrations of circulating RBC & shorter life span of RBC (70-90days) • Liver’s ability to conjugate bilirubin reduced – due to limited production of glucoronyl transferase • Lower plasma binding capacity for bilirubin because of lower albumin concentrations than other children.
  • 39. HYPERBILIRUBINEMIA POSSIBLE CAUSES: • PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): • Primary Mechanism : enterohepatic circulation/shunting • Normally: Conjugated bilirubin  urobilinogen (excreted) • Sterile & less motile NB bowel is less effective in excreting urobilinogen • Conjugated bilirubin thru B-glucoronidase converted back to unconjugated bilirubin reabsorbed by intestinal mucosa  liver
  • 40. HYPERBILIRUBINEMIA POSSIBLE CAUSES: • An association with breast feeding or breast milk • BREASTFEEDING JAUNDICE – early onset • Begins at 2-4days of age; 12-13% of Breastfeeding infants • Related to process of breastfeeding, results from decreased caloric & fluid intake by Breastfeeding infants before milk supply is well-established (fasting is associated with decrease hepatic clearance of bilirubin) • Feeding (+) peristalsis  more rapid passage of meconium decreased amount of reabsorption of unconjugated bilirubin • Feeding introduces bacteria to aid in reduction of bilirubin to urobilinogen • Colostrums, natural cathartic, facilitates meconium evacuation
  • 41. HYPERBILIRUBINEMIA POSSIBLE CAUSES: • An association with breast feeding or breast milk • BREAST MILK JAUNDICE – late onset • Onset: 4th-7th day of age; 12-13% of Breastfeeding infants • Rising levels peak at 2nd week  gradually diminish • May remain jaundiced x 3-12 weeks or more  infants are well • May be caused by factors in BM (pregnanediol, fatty acids, B-glucorinidase) that either inhibit conjugation or decrease excretion of bilirubin • Less frequent stooling by Breastfeeding infants may allow for extended time for reabsorption of bilirubin from stools
  • 42. HYPERBILIRUBINEMIA POSSIBLE CAUSES: • Excess production of bilirubin – Hemolytic disease, biochemical defects, bruises • Hemolytic disease – blood antigen incompatibility – hemolysis of RBC ; liver unable to conjugate & excrete excess bilirubin from hemolysis • Onset: 1st 24 hours (levels increase faster than 5mg/dl/day) • Treatment: Postnatal – phototherapy ; exchange transfusion – severe • Prenatal – transfusion (fetus) ; Rhogam
  • 43. HYPERBILIRUBINEMIA POSSIBLE CAUSES: • Disturbed capacity of liver to secrete conjugated bilirubin – enzyme deficiency, bile duct obstruction • Combined overproduction & undersecretion – sepsis • Some disease states – hypothyroidism, galactosemia, infant of a diabetic mother • Genetic predisposition to increase production – Native Americans, Asians
  • 44. HYPERBILIRUBINEMIA CLINICAL MANIFESTATIONS • Jaundice – most obvious sign • Yellowish discoloration: sclera, nails, skin • If it appears within 1st 24 hours: hemolytic disease of Newborn, sepsis, maternally- derived diseases (DM, infections) • Appears on 2nd or 3rd day, peaks on 3rd – 4th day, declines on 5th – 7th day: physiologic jaundice (varies according to ethnicity) • Intensity of jaundice is not always related to the degree of hyperbilirubinemia
  • 45. HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION • Serum Bilirubin (B1: 0.2-1.4mg/dl) • Jaundice appears at >5mg/dl • Evaluation based on: • Timing of appearance of clinical jaundice • Gestational age at birth • Age in days since birth • Family history including maternal Rh factor • Evidence of hemolysis • Feeding method • Infant’s physiologic status • Progression of serum bilirubin levels
  • 46. HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION • Indicators of physiologic jaundice – warrants further investigation as to the cause of jaundice • Clinical jaundice within 24 hrs. of birth • Persistent jaundice over 2 weeks in full-term, formula fed infant • Total serum bilirubin levels 12.9mg/dl (term infant) or over 15mg/dl (preterm); upper limit for breastfeeding infant – 15mg/dl • Increase serum bilirubin >5mg/dl/day • Direct bilirubin (B2) 1.5-2mg/dl • Total serum Bilirubin – over 95th percentile for age (in hours) on hour-specific risk nomogram
  • 47. HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION • Transcutaneous Bilirubinometry – noninvasive monitoring of bilirubin via cutaneous reflectance mechanisms; allow for repetetive estimations of bilirubin • Hour-specific Serum Bilirubin Levels – predict newborn at risk for rapidly rising levels • Recommended by AAP for monitoring healthy Newborn >35wks AOG before discharge from hospital • Carbon monoxide indices in exhaled breath – CO is produced when RBC is broken down
  • 48. HYPERBILIRUBINEMIA COMPLICATIONS • BILIRUBIN ENCEPHALOPATHY/ KERNICTERUS – unconjugated bilirubin highly toxic to the neurons • Syndrome of severe brain damage due to deposition of unconjugated bilirubin in brain cells (extremely high B1 level increase crosses the blood-brain barrier) • KERNICTERUS – yellow staining of brain cells that may result in bilirubin encephalopathy
  • 49. HYPERBILIRUBINEMIA COMPLICATIONS • FACTORS THAT CONTRIBUTE TO BILIRUBIN NEUROTOXICITY: • Serum bilirubin alone do not predict the risk of brain injury • Metabolic acidosis • Low serum albumin level • Intracranial infections (meningitis) • Abrupt increase in BP • Conditions that increase metabolic demands for oxygen and glucose – fetal distress, hypoxia, hypothermia, hypoglycemia
  • 50. HYPERBILIRUBINEMIA COMPLICATIONS • SIGNS OF CNS DEPRESSION/ EXCITATION: • Prodrome: decreased activity, lethargy, irritability, hypotonia, seizures • Athetoid CP, mental retardation, deafness • Those who survived: NEUROLOGIC DAMAGE • Mental retardation, ADHD, delayed/ abnormal motor movements (ataxia, athetosis), behavior disorders, perceptual problems, sensorineural hearing loss
  • 51. HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Phototherapy – main form • Exchange transfusion – reduce high bilirubin levels that occur with hemolytic disease • Phenobarbital – hemolytic disease; effective when given to mother several days before delivery • Promotes hepatic glucoronyl transferase synthesis  increases bilirubin conjugation & hepatic clearance of pigment in bile • Promotes protein synthesis – increase albumin for more bilirubin binding sites • Heme-oxygenase inhibitors – decrease bilirubin production
  • 52. HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Early initiation of feedings & frequent breastfeeding – promotes increased intestinal motility, decreases enterohepatic shunting, establish normal bacterial flora in the bowel excrete B2 • Frequent breastfeeding every 2 hrs • Avoid glucose water, formula or water supplementation
  • 53. HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Phototherapy – application of fluorescent light (bili light) to infant’s exposed skin • Light  promotes bilirubin excretion by photoisomerization (alters structure of bilirubin to a soluble form – lumirubin) for easier excretion • Blue Light – more effective in reducing bilirubin but alters the color of the infant • Fluorescent bulbs with spectrum 420-460nm preferred • Infant skin is fully exposed
  • 54. HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT • Phototherapy – application of fluorescent light (bili light) to infant’s exposed skin • Rapidly rising bilirubin/ critical level – double intensive phototherapy • Conventional overhead lamps while infant is lying on fiber optic blanket • BEST RESULT: occur within 1st 24-48hrs of treatment • Fiberoptic blanket/panel – light generating illuminator • blanket delivers therapeutic light consistently & continuously to infant & achieve same photoisomerization as conventional phototherapy • For home phototherapy, permits more infant-parent interaction, better temperature control • Eliminates the need for eye patches • SPECIAL CAUTION: plastic pad must completely be covered to prevent exposing fragile skin of extremely immature/compromised infant to fiberoptic blanket (dermal injury) • When blood is drawn, phototherapy lights are turned off, blood is transported in covered tube to avoid false reading as a result of bilirubin destruction in test tube.
  • 55. HYPERBILIRUBINEMIA AGE (HOURS) CONSIDER PHOTOTHERAPY PHOTOTHERAPY EXCHANGE TRANSFUSION IF INTENSIVE PHOTOTHERAPY FAILS EXCHANGE TRANSFUSION AND INTENSIVE PHOTOTHERAPY 24 --- --- --- --- 25-48 >/= 12 (170) >/= 15 (260) >/= 20 (340) >/= 25 (430) 48-72 >/= 15 (260) >/= 18 (310) >/= 25 (430) >/= 30 (510) >72 >/= 17 (290) >/= 20 (340) >/= 25 (430) >/= 30 (510) MANAGEMENT OF HYPERBILIRUBINEMIA IN HEALTHY TERM NEWBORN TSB LEVEL (mg/dl/mmol/L)
  • 56. HYPERBILIRUBINEMIA PROGNOSIS: • Early recognition prevents brain damage • Bilirubin encephalopathy: athetosis, sensorineural hearing loss, paralytic gaze palsy, gaze abnormalities, delayed motor skills, dental enamel hypoplasia
  • 57. HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • ASSESSMENT • Observe for evidence of jaundice at regular intervals • Observe color from head-toe, color of sclera & mucous membranes • Apply direct pressure to skin especially bony prominences (tip of nose or sternum)  blanching  allow yellow stain to be more pronounced • Dark-skinned – color of sclera, conjunctiva, oral mucosa • Observe natural daylight • Evidence of jaundice that appears before infant is 24 hrs of age – indication for assessing bilirubin levels
  • 58. HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • Phototherapy – nude under light source, repositioned frequently to expose all body surface areas to light • Frequent bilirubin determination – every 6-12hrs (visual assessment is no longer considered valid)
  • 59. HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • PHOTOTHERAPY: • PRECAUTIONS: • Eye Shield – opaque mask to prevent exposure to light • Properly sized, correctly positioned without occluding the nares • Infant’s eyelids are closed before mask is applied, corneas may become excoriated • Eyes checked every shift for discharge, excessive pressure on lids, corneal irritation • Removed during feedings • Infants in open crib must have a protective plexiglass shield between them & fluorescent lights to minimize amount of undesirable UV lights reaching skin & protect them from accidental bulb breakage • Temperature monitored • Maintain in flexed position w/ rolled blankets alongside body
  • 60. HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • PHOTOTHERAPY: • ACCURATE CHARTING: • Times that phototherapy is started and stopped • Proper shielding of the eyes • Type of fluorescent lamp • Number of lamps • Distance between surface of lamps & infant (not <18 in) • Use of phototherapy in combination with an incubator or open bassinet • Photometer measurement of light intensity • Occurrence of side effects • Side effects: loose greenish stools transient skin rashes, hypothermia, Increase BMR, DHN, electrolyte imbalance (hypocalcemia), priapism
  • 61. HYPERBILIRUBINEMIA NURSING CONSIDERATIONS • PHOTOTHERAPY: • Informed consent prior to treatment • Oily lubricants/lotions not used – “frying effect” • Full-term newborn – additional fluid volume to compensate for fluid loss • Meticulous skin care • Rebound effect – after phototherapy is permanently discontinued  subsequent increase in serum bilirubin level; transient • “Bronze Baby Syndrome” – serum, urine, skin turn grayish brown hours after infant is placed under light • Due to retention of bilirubin breakdown product of phototherapy (copper prophyrin) • Infants with elevated B2 level & some degree of cholestasis • Resolves after discontinuation of phototherapy
  • 62.
  • 63. RESPIRATORY DISTRESS SYNDROME (RDS) • Condition of surfactant deficiency & physiologic immaturity of thorax • Seen almost exclusively in preterm infants; seen in infants <32 wks AOG • A disease related to developmental delay in lung maturation • Also associated with multifetal pregnancies, infants of diabetic mothers, Caesarean Section delivery, delivery before 37 weeks AOG, low birth weight, precipitous delivery, cold stress, asphyxia, history of previous RDS • Rare in drug-exposed infants or those who have been exposed to chronic intrauterine stress (HPN, preeclampsia) • RDS of nonpulmonary origin in Newborn: sepsis, cardiac defects, exposure to cold, airway obstruction, IVH, hypoglycemia, metabolic acidosis, acute blood loss, drugs.
  • 64. RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY Deficient Surfactant Collapse of Alveoli Great deal of effort to reexpand the alveoli with each breath Exhaustion Fewer and fewer alveoli opens Atelectasis Hypoperfusion to the lung tissue Hypoxemia and hypercapnia
  • 65. RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Preterm – born before lungs are fully prepared for gas exchange (critical factor in RDS) • Combination of structural and functional immaturity of lungs • (+) fetal respiratory activity before birth: lungs have feeble respiratory movements, fluid excreted thru alveoli
  • 66. RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Final unfolding of alveolar septa (increase surface area of the lungs) occurs on last trimester of pregnancy Preterms are born with underdeveloped and uninflatable alveoli Limited pulmonary blood flow Collapsed lungs Increased pulmonary vascular resistance Fetal blood shunted from lungs by ductus arteriosus and foramen ovale
  • 67. RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Rib Cage: weak and compliant • Fetal chest highly compliant because of predominance of cartilage; diaphragm is prone to fatigue • Fetal Lungs deficient in surfactant due to immaturity of surfactant producing type 2 alveolar cells • Surfactant – 1st produced at 24 wks AOG, type 2 cells do not fully mature until about 36 wks AOG • Reduces surface tension of fluids that line the alveoli & respiratory passages  uniform expansion and maintains lung expansion
  • 68. RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY • Deficient surfactant – unequal inflation of alveoli on inspiration, collapse of alveoli of end expiration • Without surfactant – infants unable to keep lungs inflated, exerts great effort to reexpand the alveoli  exhaustion  atelectasis
  • 69. RESPIRATORY DISTRESS SYNDROME (RDS) • PATHOPHYSIOLOGY Inadequate pulmonary perfusion and ventilation Hypoxemia and hypercapnia Markedly reactive pulmonary arterioles and thick Muscular layer decreased oxygen concentration Decreased oxygen tension + decreased blood pH Vasospasm in pulmonary arterioles Increased PVR Intrapulmonary shunting Anaerobic glycolysis Metabolic acidosis, cyanosis
  • 70. RESPIRATORY DISTRESS SYNDROME (RDS) MAJOR FACTORS IN RDS CAUSE EFFECT Increased surface tension of alveoli (surfactant deficiency) Alveolar collapse, atelectasis, increased difficulty in breathing Impaired gas exchange Hypoxemia, and hypercapnia with respiratory acidosis Increased pulmonary vascular resistance Hypoperfusion of pulmonary circulation Hypoperfusion (with hypoxemia) Tissue hypoxia & metabolic acidosis Increased transudation of fluid into lungs Hyaline membrane formation; impaired gas exchange • PATHOPHYSIOLOGY • (+) pulmonary edema – impaired gas exchange • (+) pulmonary interstitial emphysema – overdistention of distal airways
  • 71. RESPIRATORY DISTRESS SYNDROME (RDS) • CLINICAL MANIFESTATIONS: • Respiratory Signs and Symptoms: • Tachypnea (80-120/min) initially : dyspnea • Pronounced intercostals and/or substernal retractions • Fine inspiratory crackles ; audible expiratory grunt • Flaring of external nares • Cyanosis / pallor • As disease progresses • Apnea ; flaccidity ; absent spontaneous movement • Unresponsive ; diminished breath sounds ; mottling • Severe disease: shock-like state • Decreased cardiac output and bradycardia • Low systemic BP
  • 72. RESPIRATORY DISTRESS SYNDROME (RDS) • EVALUATION: • Blood glucose test • Chest x-ray with fine, diffuse, recticogranular or “ground glass appearance and air bronchogram • Arterial blood gas (ABGs) ; pulse oximetry and carbon dioxide monitoring, pulmonary function tests
  • 73. RESPIRATORY DISTRESS SYNDROME (RDS) • EVALUATION: • Prenatal diagnosis: • Problems like maternal diabetes – delay fetal lung maturation • Antenatal administration of glucocorticoids – enhance fetal lung maturation • Lecithin / sphingomyelin ratio (L:S ratio) : relationship between these 2 lipids during gestation • L:S = 2:1 • “Shake/ bubble test” – stable foam bubbles form when amniotic fluid is shaken in presence of ethanol • Tap Test – abundant bubbles appear in test tube of amniotic fluid with 6N – HCL and diethyl ether • TDx fetal lung maturity assay
  • 74. RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • Immediate establishment of adequate oxygen and ventilation and supportive measures required for a preterm, prevent further complications • SUPPORTIVE MEASURES: • Maintain adequate ventilation and oxygen • Maintain acid-base balance • Maintain neutral thermal environment • Maintain adequate tissue perfusion and oxygen • Prevent hypotension • Maintain adequate hydration and electrolyte status • NUTRITION: parenteral therapy during 1st phase of disease • Nipple and gavage feedings are contraindicated – causes increase RR, prone to aspiration • Enteral substrate to infant with transient hypoxia – increase risk Necrotizing Enterocolitis
  • 75. RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • EXOGENOUS SURFACTANT REPLACEMENT (via ET Tube) • Decrease oxygen requirements and mean airway pressure (MAP) • Improves blood gas values & ventilator settings • Decrease incidence of pulmonary air leaks • Decrease deaths from RDS • Decrease mortality rate • COMPLICATIONS: pulmonary hemorrhage, mucous plugging • Given at birth via endotracheal (ET) tube directly into infants trachea • NURSING RESPONSIBILITIES: • Assist in delivery of the product, collection, and monitoring of ABG’s, scrupulous monitoring of oxygen with pulse oximetry • Assess infant’s tolerance of procedure • Delay suctioning for an hour or so to allow maximum effects to occur
  • 76. RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • OXYGEN THERAPY • Aggressive respiratory support: Oxygen, continuous positive airway pressure (CPAP), intubation, mechanical ventilation • Goals of Oxygen therapy: provide adequate oxygen to tissues • Prevent lactic acidosis resulting from hypoxia • Avoid negative effects of oxygen barotrauma / toxicity • Gas should be warmed before entering respiratory tract • Oxygen can be supplied via plastic hood • If oxygen saturation of blood cannot be maintained at satisfactory level and PaO2 rises  ventilatory assistance
  • 77. RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED CONVENTIONAL METHODS Continuous Positive Airway Pressure (CPAP) Provides contrast distending pressure to airway in spontaneously breathing infant. Nasal prongs, endotracheal tube, face mask, nasal cannula Positive End-Expiratory Pressure (PEEP) Provides increase end-expiratory pressure during expiration and between Mandatory breaths which prevents alveolar collapse; maintains residual airway pressure Endotracheal intubation, and either volume-limited or pressure-limited ventilator • TREATMENT / MANAGEMENT:
  • 78. RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED Intermittent Mandatory Ventilation (IMV) Allows infant to breath spontaneously at own rate but provides mechanical cycled respirations and pressure at regular preset intervals Endotracheal intubation and ventilator Synchronized Intermittent Mandatory Ventilation (SIMV) Mechanically delivered breaths are synchronized to the onset of spontaneous patient breaths; assist/control mode facilities full inspiratory synchrony; involves signal detection of onset of spontaneous respiration from abdominal movement, thoracic impedance, airway pressure, or flow changes Patient-triggered infant ventilator with signal detector and assist/control mode; endotracheal tube • TREATMENT / MANAGEMENT:
  • 79. RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED Volume Guarantee Ventilation Delivers predetermined volume of gas using an inspiratory pressure that varies according to infant’s lung compliance (often used in conjunction with SIMV) Volume guarantee ventilator with flow sensor; endotracheal tube ALTERNATIVE METHODS High frequency Oscillation (HFO) Application of high-frequency, low- volume, sine wave flow oscillations to airway at rates between 480 and 1200 breaths/min Variable-speed piston pump (or loudspeaker, fluidic oscillator) ; endotracheal tube • TREATMENT / MANAGEMENT:
  • 80. RESPIRATORY DISTRESS SYNDROME (RDS) METHOD DESCRIPTION HOW PROVIDED High-Frequency Jet Ventilation (HFJV) Uses separate, parallel, low compliant circuit and injector port to deliver small pulses or jets of fresh gas deep into airway at rates between 250 and 900 breaths/min May be used alone or with low-rate IMV; endotracheal tube • TREATMENT / MANAGEMENT:
  • 81. RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • COMPLICATIONS OF POSITIVE PRESSURE VENTILATION: • Increased incidence of air leaks that produce complications: • Pulmonary Interstitial Emphysema • Pneumothorax • Pneumomediastinum • Associated with Intubation: • Nasal/tracheal/pharyngeal perforation • Stenosis; inflammation • Palatal grooves; subglottic stenosis • Tube obstruction and infection
  • 82. RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • INHALED NITRIC OXIDE (NO): for newborn with conditions that cause persistent pulmonary HPN, pulmonary vasoconstriction, subsequent acidosis, and severe hypoxia • Colorless, highly diffusible gas: cause smooth muscle relaxation and reduce pulmonary vasoconstriction and subsequent pulmonary HPN when inhaled into lungs • Administered through ventilator circuit and blended with oxygen • Attaches readily to hemoglobin and deactivated so that systemic vasculature is not affected • Toxic in large quantities • Mucus may collect I respiratory tract as a result of infant’s pulmonary condition  interferes with gas flow and obstruct passages • Catheter inserted gently but quickly; intermittent suctioning (limited to <5secs) • FiO2 increased by 10% before suctioning
  • 83. RESPIRATORY DISTRESS SYNDROME (RDS) • TREATMENT / MANAGEMENT: • Most advantageous position for facilitating an infant’s open airway are on the side with head supported in alignment by small folded blanket • Back position – keep neck slightly extended • Head in “sniffing” position • Inspection of skin – position changes and use of water pillows (prevents skin breakdown) • Mouth care
  • 84. RESPIRATORY DISTRESS SYNDROME (RDS) • TRANSIENT TACHYPNEA OF THE NEWBORN (RDS TYPE 2) • Delayed resorption of fetal lung fluid; decrease lung compliance • Management: Oxygen therapy • Signs and symptoms similar to RDS 1 (hyaline membrane disease) but resolves 48-72 hrs.
  • 85.
  • 86. SEPSIS / SEPTICEMIA • Generalized bacterial infection in the bloodstream • Newborns are highly susceptible to infection as a result of diminished nonspecific (inflammatory) & specific (humoral) immunity: impaired phagocytosis, delayed chemotactic response, minimal/absent IgA & IgM, decreased complement levels • High-Risk Infant 4x greater chance; males > females
  • 87. SEPSIS / SEPTICEMIA • RISK FACTORS: • Prematurity • Congenital Anomalies • Acquired injuries that disrupt the skin, mucous membranes • Invasive procedures – IV lines, ET tubes • Administration of TPNs • Nosocomial exposures – NICU • Infant born after a difficult or traumatic labor & delivery
  • 88. SEPSIS / SEPTICEMIA • PATHOPHYSIOLOGY: • Premature withdrawal of placental barrier – leaves infants vulnerable to viral, fungal, bacterial, parasitic infections • Early birth interrupts transplacental transmission of passive immunity (IgG) • Preterms – low IgG; IgA & IgM not transferred to fetus
  • 89. SEPSIS / SEPTICEMIA • SOURCES OF INFECTION: • Acquired prenatally across placenta from maternal blood stream or during labor from ingestion or aspiration of infected amniotic fluid • Prolonged rupture of membranes – maternal-fetal transfer of pathogenic organisms • Transplacental transfer of CMV, toxoplasmosis, syphilis can occur
  • 90. SEPSIS / SEPTICEMIA • SOURCES OF INFECTION: • Early Sepsis (< 3days) – acquired in perinatal period • Direct contact with organisms from maternal GIT & GUT • Group B streptococcus (GBS), E. Coli • H. influenza, coagulase-negative staphylococci – Very Low Birth Weight infants • Gonococci, Candida albicans, Herpes Simplex Virus II, Listeria organism, Chlamydia • Late Sepsis (1-3 weeks after birth) – nosocomial • Staphylococci, Kleibsiella, enterococci, Pseudomonas • Coagulase-negative staphylococci – Extremely Low Birth Weight, Very Low Birth Weight Infants
  • 91. SEPSIS / SEPTICEMIA • SOURCES OF INFECTION: • Bacterial Invasion: umbilical stump, mucous membranes of the eyes, nose, pharynx, ear; internal systems (respiratory, nervous, urinary, GIT) • Postnatal Infection: cross-contamination from other infants, personnel, object in the environment
  • 92. SEPSIS / SEPTICEMIA • SIGNS AND SYMPTOMS: • Systemic Infections – subtle, vague, nonspecific • General: Fever, Temperature instability; “not doing well”; poor feeding, edema • GI System: poor feeding, abdominal distention; vomiting; diarrhea/ decreased stooling; Hepatomegaly, hemoccult-positive stools • Respiratory System: irregular respirations, Apnea/tachypnea; dyspnea, retractions; flaring, grunting; cyanosis • Renal System: Oliguria
  • 93. SEPSIS / SEPTICEMIA • SIGNS AND SYMPTOMS: • Cardiovascular System/ Circulatory: Pallor/ cyanosis/ mottling, cold clammy skin; hypotension; irregular heartbeat : Tachycardia/ Bradycardia, edema • CNS: diminished activity – lethargy, hyporeflexia, coma • Increased activity – irritability, tremors, seizures • Full fontanelle, High-pitched cry, increased/ decreased tone, abnormal eye movements • Hematologic System: Jaundice, splenomegaly, pallor, petechiae, purpura, ecchymosis
  • 94. SEPSIS / SEPTICEMIA • DIAGNOSIS: • Based on suspicion of presenting clinical signs and symptoms • Laboratory and radiographic examination – definitive diagnosis • Blood/ urine/ CSF cultures – 10% will have negative cultures • CBC: anemia, leukocytosis/ leucopenia • Leucopenia – ominous sign • C-reactive protein serial measurements • Chest x-ray • Lumbar puncture if < 28 days old, and if with altered mental status or meningeal signs
  • 95. SEPSIS / SEPTICEMIA • THERAPEUTIC MANAGEMENT: • SUPPORTIVE THERAPY: Circulatory, respiratory • Respiratory distress/ hypoxia : Oxygen therapy • IVF regulation • Correct electrolytes and acid-base balance • NPO temporarily • Blood transfusions for anemia and shock • Vital signs, thermoregulation • Aggressive administration of antibiotics, immunotherapy • Antibiotics X7-10 days if cultures are positive, discontinue in 3 days if culture is negative & infant is asymptomatic (thru IV infusion) • Antifungal/ antiviral therapies
  • 96. SEPSIS / SEPTICEMIA • PROGNOSIS • Variable • ELBW/ VLBW infants: Early onset sepsis  severe neurologic & respiratory sequelae • Late-onset sepsis & meningitis: poor outcome
  • 97. SEPSIS / SEPTICEMIA • NURSING CONSIDERATIONS: • Recognize existing problem: “something is wrong” • Awareness of potential modes of infection transmission • Knowledge of the side effects of specific antibiotic & proper regulation & administration of drug are vital • Prolonged antibiotic therapy – (+) growth of resistant organisms & superinfection from fungal/ mycotic agents (Candida albicans) • Nystatin oral suspension swabbed on oral mucosa – prophylaxis • Avoid fully flexed position for obtaining spinal fluid.
  • 98. SEPSIS / SEPTICEMIA • NURSING CONSIDERATIONS: • Continual cardiorespiratory & pulse oximetry monitoring provides an ongoing assessment of infant’s condition • Decrease additional physiologic or environmental stress • Thermoregulated environment • Anticipate potential problems – dehydration, hypoxia • Precautionary measures: proper hand washing, use disposable equipment • Proper disposal of excretions (vomitus, stool) • Adequate housekeeping • Observe for signs of complications – meningitis, septic shock
  • 99.
  • 100. NECROTIZING ENTEROCOLITIS • Acute inflammatory disease of the bowel • Seen primarily in premature infants, although, described in full-term neonates as well • Occurs several weeks after birth • ETIOLOGY: • Precise Cause: unknown • Prematurity: risk factor
  • 101. NECROTIZING ENTEROCOLITIS • ETIOLOGY: • 3 FACTORS THAT PLAY ROLE IN DEVELOPMENT OF NEC: • Intestinal Ischemia – vascular compromise on GIT Diminished Blood Supply Cell death No secretion of protective, lubricating mucus Thin unprotected wall attacked by proteolytic enzyme Bowel wall swell and break down Unable to synthesize IgM, mucosa permeable to toxins Gas-forming bacteria invasion (+) pneumatosis intestinalis (air in submucosa / subserosa)
  • 102. NECROTIZING ENTEROCOLITIS • ETIOLOGY: • 3 FACTORS THAT PLAY ROLE IN DEVELOPMENT OF NEC: • Colonization by pathogenic bacteria • Substrate (formula feeding) in intestinal lumen – stress on ischemic bowel • SIGNS AND SYMPTOMS: • Nonspecific Clinical Signs: • Lethargy, poor feeding, hypotension • Vomiting, oliguria, hypotension • Unstable temperature, jaundice
  • 103. NECROTIZING ENTEROCOLITIS • SIGNS AND SYMPTOMS: • Specific Signs: • Distended (often shiny) abdomen; blood in stools/gastric content • Gastric retention; bilious vomitus • Localized abdominal wall erythema/ induration • DIAGNOSIS: • Abdominal x-ray: Sausage-shaped dilation of intestine  distended loops of bowel; “pneumatosis intestinalis” --- “soapsuds” or bubbly appearance of thickened bowel wall & ultralumina; • Air in portal vein; free air under the diaphragm (perforation)
  • 104. NECROTIZING ENTEROCOLITIS • DIAGNOSIS: • Occult blood in the stool • Blood culture – bacteremia / septicemia • CBC: anemia, leucopenia/ leukocytosis • Metabolic acidosis, electrolyte imbalance • TREATMENT: • Begins with prevention • NPO x 24-48 hours – infants who have suffered birth asphyxia, ELBW, VLBW infants • Breast milk • Minimal enteral feedings – trophic feeding, GIT priming
  • 105. NECROTIZING ENTEROCOLITIS • TREATMENT: • Confirmed NEC: • Discontinue all oral feedings • Place NGT – for decompression • IV fluids; IV antibiotics • Surgery in extreme cases • PROGNOSIS: • Sequelae of surgical intervention: shirt-gut syndrome, colonic stricture with obstruction, fat malabsorption, failure to thrive
  • 106. NECROTIZING ENTEROCOLITIS • NURSING CONSIDERATIONS: • Prompt recognition of early warning signs of NEC: abdominal distention, absent bowel sounds • Measure abdominal girth, residual gastric contents before feedings, listen for presence of bowel sounds • Vital signs including blood pressure • Avoid rectal temperatures (danger of perforation) • Avoid pressure on distended abdomen • Infants are left undiapered & positioned supine or on the side • Conscientious attention to nutritional and hydration needs, administration of antibiotics • Oral feedings: started 7-10 days after diagnosis & treatment using human milk, elemental formula • Sterile water may be given initially • Strict hand washing
  • 107.
  • 108. FAILURE TO THRIVE • Sign of inadequate growth resulting from inability to obtain or use calories required for growth • No universal definition • Common parameter: WEIGHT, sometimes height that falls below 5th percentile for child’s age • Weight for age (height) z value of less than -2.0 • Weight curve (loss) that crosses >2 percentile lines on National Center for Health Statistics (NCHS) growth after previous achievement of a stable growth pattern.
  • 109. FAILURE TO THRIVE • 3 GENERAL CATEGORIES: • Organic Failure to Thrive • Physical Cause • Congenital heart defects, neurologic lesions, cerebral palsy, microcephaly • Chronic renal failure, gastroesophageal reflux • Malabsorption syndrome, endocrine dysfunction • Cystic fibrosis, acquired immunodeficiency syndrome (AIDS) • Nonorganic Failure to Thrive (NFTT) • Unrelated to disease • Result of psychosocial factors – inadequate nutritional information by parent • Deficiency of maternal care of disturbance in maternal-child attachment • Disturbance in child’s ability to separate from parent leading to food refusal to maintain attention • Idiopathic Failure to Thrive – unexplained by usual organic and environmental etiologies but may also be classified as NFTT.
  • 110. FAILURE TO THRIVE • Some experts suggest that classifications are too simplistic because most cases of growth failure have mixed causes. • FTT be classified according to pathophysiology for the following categories: • Inadequate Caloric Intake • Incorrect formula preparations • Neglect, food fads • Excessive juice consumption • Poverty • Behavioral problems affecting eating • CNS problems affecting intake
  • 111. FAILURE TO THRIVE • Inadequate absorption • Cystic fibrosis, celiac disease, vitamin/ mineral deficiencies, biliary atresia, hepatic disease • Increase metabolism • Hyperthyroidism, congenital heart defects, chronic immunodeficiency • Defective utilization • Trisomy 21 or 18, congenital infection, metabolic storage diseases
  • 112. FAILURE TO THRIVE • ETIOLOGY – multifactorial • Infant organic disease • Dysfunctional parenting behaviors • Subtle neurologic/ behavioral problems • Disturbed parent-child interactions • FACTORS LEADING TO INADEQUATE FEEDING OF INFANT • Poverty – dilute formula to extend available supply; no insurance • No primary care practitioner; homelessness
  • 113. FAILURE TO THRIVE • Health or childbearing beliefs – fad diets, excessive concern with obesity, hypercholesterolemia, nursing caries • Strict use of scheduled feedings • Inappropriate food source; excessive juice intake • Inadequate nutritional knowledge – cultural confusion (immigrant to USA); cognitive impairments • Family Stress – overwhelming involvement with another chronically ill child • Financial, marital, excessive parenting & employment responsibilities • Single parent employed full time, depression, substance abuse, acute grief
  • 114. FAILURE TO THRIVE • Psychosocial factors – maternal depression, Munchausen syndrome by proxy, child temperament • Feeding resistance – oral tactile hypersensitivity • Infant receiving nonoral nutritional therapy early in life or exclusively fed with feeding tubes • Insufficient breast milk – fatigue, poor release of milk, breast surgery augmentation, lack of maternal confidence / support.
  • 115. FAILURE TO THRIVE • CLINICAL MANIFESTATIONS: • Growth Failure – 5th percentile in weight only or weight and height • Developmental delays – social, motor, adaptive, language • Apathy • Poor hygiene • Withdrawn behavior • Feeding/ eating disorder: vomiting, anorexia, pica, rumination • No fear of strangers (stage when stranger anxiety is normal) • Avoidance of eye contact • Wide-eyed gaze & continual scan of environment (radar gaze) • Stiff & unyielding or flaccid & unresponsive • Minimal smiling
  • 116. FAILURE TO THRIVE • DIAGNOSTIC EVALUATION: • Evidence of growth retardation & caloric deprivation • Anthropometric measurements • Onset of FTT is fairly recent: weigh (not height) is below accepted standards (5th percentile) • Long standing FTT: height and weight depressed; chronic malnutrition • Complete health and dietary history --- history of food consumed over 3-5 day period • Child’s activity level, perceived food allergies, dietary restrictions • P.E for evidence of organic causes, developmental assessment • Family assessment – parental height, household organizations & mealtime behaviors & rituals • Rule out organic causes • Lead toxicity, anemia, stool-reducing substance, occult blood, ova, parasites • Alkaline phospatase, zinc levels
  • 117. FAILURE TO THRIVE • THERAPEUTIC MANAGEMENT: • Directed as reversing the malnutrition & underlying cause • Goal: provide sufficient calories to support “catch up” growth • Treat any coexisting problems • Multidisciplinary team: physician, nurse, dietitian, gastroenterologist, child- life specialist, social worker or mental health professional • Relieve any additional stresses on family – referrals to welfare agencies or supplemental food programs
  • 118. FAILURE TO THRIVE • THERAPEUTIC MANAGEMENT: • Family therapy • Behavior modification • Hospitalization indications: • Evidence (anthropometric) of severe acute malnutrition • Child abuse / neglect • Significant dehydration • Caretaker substance abuse or psychosis • Outpatient management that does not result in weight gain
  • 119. FAILURE TO THRIVE • NURSING CONSIDERATIONS: • Accurate assessment of initial weight & height and daily weight & recording of all food intake • Feeding behavior is documented & parent-child interaction during feeding • Feeding checklist • Should be placed in a room with noninfectious children of similar age • Structure feeding environment to encourage eating
  • 120. FAILURE TO THRIVE • NURSING CONSIDERATIONS: • The child • May exhibit altered behavioral interactions • Display intense interest in inanimate objects (toys) but less in social interactions • Watchful of people at a distance but become distressed as others come closer • Dislike being touched or held & avoid face-to-face contact; when held they protest briefly on being put down& apathetic when left alone • History of difficulty in feeding, vomiting, sleep disturbance, excessive irritability • Crying during feedings, hoarding food in mouth, rumination after feeding, refusing to switch from liquids to solids, aversion behaviors (turning from food, spitting) • Difficult temperament or passive, sleepy, lethargic infant who does not wake up for feedings
  • 121. FAILURE TO THRIVE • NURSING CONSIDERATIONS: • The parent • Increased risk for altered parent-infant interactions because: • Isolation and social crisis • Inadequate support systems • Poor / absent parenting role models when they were children • Lack of education, physical/ mental health problems • Physical and sexual abuse, depression, drug dependence, immaturity
  • 122. FAILURE TO THRIVE • NUTRITIONAL MANAGEMENT: • 4 Primary Goals in Nutritional management of FTT: • Correct nutritional deficiencies & achieve ideal weight for height • Increase caloric intake in formula fed infants: supplements like Polycose, medium chain triglycerides may be added slowly – in 2kcal/oz increments q2-3 days to yield up 28-30 kcal/oz • Carbohydrate additives (8 kcal/tsp)
  • 123. FAILURE TO THRIVE • NUTRITIONAL MANAGEMENT: • Rice cereal & vegetable oil • Multivitamin supplementation – zinc and iron • Breast-fed infants: add 1 tsp of 24 kcal/oz formula to 3 oz breast milk • Toddlers: high caloric milk (PediaSure) • Fruit juices – minimized in infants < 6 months • Extreme cases: tube feedings or IV therapy • Allow for catch up growth • Restore optimum body composition
  • 124. FAILURE TO THRIVE • NUTRITIONAL MANAGEMENT: • Educate parents/ primary caregivers regarding child’s nutritional requirements & appropriate feeding methods • Step-by-step directions for formula preparations, written schedule of feeding times • Juices should be avoided in children with growth failure until adequate weight gain has been achieved (should not exceed 4oz/day) • Family-system approach
  • 125.
  • 126. HEMOLYTIC DISEASE OF THE NEWBORN • Erythroblastosis fetalis • Hyperbilirubinemia in 1st 24 hrs of life • Abnormally rapid rate of RBC destruction • Anemia caused by this destruction (+) production of RBCs  increased # cells for hemolysis • Major causes: isoimmunization (primarily Rh) & ABO incompatibility
  • 127. HEMOLYTIC DISEASE OF THE NEWBORN • Blood Incompatibility • Antigen / Agglutinogens – substance capable of producing an immune response if recognized by the body as foreign • Antigens + Antibodies = agglutination (clumping) • Antibodies in plasma of 1 blood group (except AB group – no antibodies) produce agglutination when mixed with antigens of a different blood group • ABO blood group system – antibodies occur naturally • Rh system - isoimmunization
  • 128. HEMOLYTIC DISEASE OF THE NEWBORN 1. Rh Incompatibility • The presence of naturally occurring Rh factor determines the blood type. • Rh (+) – presence of antigen • Rh (-) – absence of antigen • No problems occur when Rh blood type are same in both mother and fetus or if mother is Rh (+) and infant is Rh (-). • Mother Rh (-) and Infant Rh (+) : problem
  • 129. HEMOLYTIC DISEASE OF THE NEWBORN • Isoimmunization – no effect on 1st pregnancy • Initial sensitization to Rh antigens rarely occurs before the onset of labor • With increased risk of fetal blood transferred to maternal circulation during placental separation, maternal antibody production is stimulated. Fetal RBCs (with antigens foreign to mother) Enters maternal circulation Mother produces anti-Rh antibodies
  • 130. HEMOLYTIC DISEASE OF THE NEWBORN • Factors that increase incidence of transpalcental hemorrhage & subsequent isoimmunization: • Multiple gestation, abruptio placenta, placenta previa, manual removal of placenta, cesarean delivery Subsequent pregnancy with Rh (+) fetus Previously formed maternal antibodies to Rh (+) blood cells enter fetal circulation Attack and destroy fetal RBCs
  • 131. HEMOLYTIC DISEASE OF THE NEWBORN • Sensitization may occur during 1st pregnancy if woman had previously received an Rh (+) blood transfusion Fetus compensate for hemolysis and anemia Increase rate of erythropoiesis (+) erythroblasts in circulation Erythroblastosis fetalis
  • 132. HEMOLYTIC DISEASE OF THE NEWBORN • No sensitization: if there’s strong placental barrier which prevents transfer of fetal blood into maternal circulation • 10-15% of sensitized mothers: no hemolytic reaction in Newborn • Some Rh (-) women even though exposed to Rh (+) fetal blood are unable to produce antibodies to foreign antigen • Most severe form: hydrops fetalis • Fetal hypoxia, cardiac failure, anasarca, effusions (pleural, pericardial, peritoneal) • Stillborn or in severe respiratory distress • Early intrauterine detection: ultrasound, fetal blood sampling • Management: fetal blood transfusions
  • 133. HEMOLYTIC DISEASE OF THE NEWBORN 2. ABO Incompatibility • Major blood group antigens of fetus are different from those of the mother • Major blood groups: A, B, AB, O • Presence / absence of antibodies & antigens determines whether agglutination will occur
  • 134. HEMOLYTIC DISEASE OF THE NEWBORN ABO RELATIONSHIP OF ANTIGENS / ANTIBODIES & DONOR- RECIPIENT COMPATIBILITY RBC COMPATIBILITY BLOOD GROUP (PHENOTYPE) GENOTYPE RBC ANTIGENS PLASMA ANTIBODIES AS DONOR TO TYPE AS RECIPIENT FROM TYPE A B AB O AA, AO BB, BO AB OO A B A & B NONE B A NONE A & B AB, A AB, B AB AB, A, B, O O, A O, B O, A, B, AB O
  • 135. HEMOLYTIC DISEASE OF THE NEWBORN Antibodies in plasma of 1 blood group (except type AB) + Antigens of a different blood group = agglutination (clumping) hemolysis Release large amounts of bilirubin into circulation
  • 136. HEMOLYTIC DISEASE OF THE NEWBORN • Most common: mother – type O and infant – type A or B • May occur in 1st pregnancy and subsequent pregnancy. Naturally occurring anti-A or anti-B antibodies Present in maternal circulation cross placenta Attack fetal RBC Hemolysis (less severe than Rh incompatibility)
  • 137. HEMOLYTIC DISEASE OF THE NEWBORN MATERNAL BLOOD GROUP INCOMPATIBLE FETAL BLOOD BROUP O B A A or B A or AB B or AB POTENTIAL MATERNAL-FETAL ABO INCOMPATIBILITIES
  • 138. HEMOLYTIC DISEASE OF THE NEWBORN • CLINICAL MANIFESTATIONS: • Anemia (hemolysis of RBCs)  jaundice on 1st 24 hours; serum bilirubin elevated (result from liver’s inability to conjugate & excrete excess bilirubin) • Hepatosplenomegaly, varying degrees of hydrops, sign of hypovolemic shock • Hypoglycemia – due to pancreatic cell hyperplasia • DIAGNOSTIC EVALUATION: • Genetic testing • Chorionic Villus Sampling – determine fetal group and type  can lead to abortion • Amniocentesis – fetal blood type  can lead to infection or leaking • Ultrasonography – allow early treatment; used to check amniotic fluid and condition of the placenta • Indirect Coombs Test – evaluate rising anti Rh antibody titers in maternal circulation; done Rh (-) mothers; 1st prenatal visit • Direct Coombs Test – detect antibodies attached to the circulating erythrocytes of affected infants ; done to baby; to determine how extensive is the hemolysis
  • 139. HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Postnatal therapy: phototherapy for mild cases, exchange transfusion for severe cases • Prevention of Rh isoimmunization: Rho immune globulin (Rhogam) • Human gamma globulin concentrate of anti-D to all unsensitized Rh (-) mothers after delivery or abortion of an Rh-positive infant or fetus • Destroys (by phagocytosis & agglutination) fetal RBCs passing into maternal circulation before they can be recognized by mother’s immune system  immune response is blocked, anti-D antibodies & memory cells not formed
  • 140. HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Must be administered to unsensitized mothers within 72 hours (possibly as long as 3-4 weeks) after the 1st delivery or abortion & repeated after subsequent ones • Administration of RhIg at 26-28 weeks AOG reduces risk of Rh isoimmunization • Administered thru IM to Rh (-) sensitized women, never to newborn or father • Intravenous immunoglobulin (IVIG) – decreased severity of RBC destruction (hemolysis) in HDN & subsequent development of jaundice • Attacks maternal cells that destroy neonatal RBCs, slows down the progression of bilirubin production • Used in conjunction with phototherapy; decreased necessity for exchange transfusion
  • 141. HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Intrauterine transfusion – infuse blood into umbilical vein of fetus • Infuse Rh O-negative packed RBCs to raise fetal hematocrit to 40-50% every 2 weeks until fetus reaches 37-38 weeks • Exchange transfusion – infant’s blood removed in small amounts (5-10ml at a time) & replaced with compatible blood (Rh – negative blood) • Removes sensitized RBCs, lowers serum bilirubin, corrects anemia, prevents cardiac failure • Indications: • Rapidly increasing bilirubin level, hemolysis despite intensive phototherapy • Infant born with hydrops fetalis or sign or cardiac failure
  • 142. HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • Fresh whole blood typed & crossmatched to mother’s serum • Amount of donor blood is double the blood volume of infant (85ml/kgBW) but not >500ml • Sterile surgical procedure: catheter  umbilical vein  inferior vena cava • 5-10 ml withdrawn within 15-20 secs  same volume x 60-90 secs
  • 143. HEMOLYTIC DISEASE OF THE NEWBORN • THERAPEUTIC MANAGEMENT: • ABO INCOMPATIBILITY • Early detection & implementation of phototherapy • (+) jaundice within 1st 24 hours, increased serum bilirubin levels, RBC spherocytosis, increased ESR: diagnostic of ABO incompatibility • IVIG + phototherapy • Exchange transfusion – not commonly required except when phototherapy fails to decrease bilirubin concentration
  • 144. HEMOLYTIC DISEASE OF THE NEWBORN • PROGNOSIS: • Severe anemia: result in stillbirth, shock, congestive heart failure, pulmonary/ cerebral complications (cerebral palsy) • With early detection & intrauterine treatment – erythroblastic Newborn rare, exchange transfusions for the conditions less common
  • 145. HEMOLYTIC DISEASE OF THE NEWBORN • NURSING CONSIDERATIONS: • Initial nursing responsibility – recognizing jaundice • Thru prenatal & perinatal history • Exchange transfusion: prepare infant and family assist practitioner with procedure • Document blood volume exchanged: amount of blood volume withdrawn & infused, time of each procedure, cumulative record of total volume exchanged • Vital signs monitored • (+) signs of cardiac/ respiratory problems: procedure stopped temporarily & resumed once stable • Observe for transfusion reaction
  • 146. HEMOLYTIC DISEASE OF THE NEWBORN • NURSING CONSIDERATIONS: • Attention on thermoregulation • Hypothermia – increase oxygen and glucose consumption  metabolic acidosis; (-) binding capacity of albumin & bilirubin & hepatic enzyme reaction  kernicterus • Hyperthermia – damages donor’s RBC, increase free K+, predisposes infant to cardiac arrest • Performed with infant under radiant warmer, with sterile drapes, blood is warmed • After procedure: nurse inspects umbilical vein (for bleeding), catheter may remain in place
  • 147.
  • 148. SUDDEN INFANT DEATH SYNDROME (SIDS) • Sudden death of infant < 1 years old • Unexplained after a complete mortem examination, including an investigation of death scene & review of case history • 3rd leading cause of death in children between 1 month – 1 year ; increased incidence in winter • Incidence: 0.65:1000 live births (1999); males > females • Peak age: 2-4 months; 95% occur by 6 months • Time of death: during sleep • Racial: Native Americans, African Americans, Hispanics • Lower socioeconomic class
  • 149. SUDDEN INFANT DEATH SYNDROME (SIDS) • Risks: Preterm especially low birth weight; multiple births (2nd twin, male twin & small-for-date twin) • Newborn with low APGAR score • Infants with CNS disturbances & respiratory disorder (bronchopulmonary dysplasia/ chronic lung disease) • Increased birth order (subsequent siblings as opposed to 1st born child) • Infants with recent history of mild illness
  • 150. SUDDEN INFANT DEATH SYNDROME (SIDS) • Sleep in prone position • Cause oropharyngeal obstruction or affect thermal balance or arousal state • Rebreathing of carbon dioxide by prone infant & impaired arousal from active & quiet sleep • Side-lying position no longer recommended – tends to turn to prone position • Use of soft bedding – not able to move their heads to the side  suffocation and lethal rebreathing • Overheating (thermal stress); co-sleeping with adult especially on sofa • Adult beds/ sofas are not designed for infants & may carry risk of accidental entrapment & suffocation
  • 151. SUDDEN INFANT DEATH SYNDROME (SIDS) • Lower incidence in breast-fed infants – pacifier may be protective against SIDS • Maternal risk: young age, cigarette smoking especially during pregnancy • Poor prenatal care, substance abuse (heroin, methadone, cocaine) • 12% of all SIDS death could be prevented with prenatal smoking cessation • Maternal smoking decreases infant’s ability to arouse to auditory stimuli in mothers who smoke prenatally.
  • 152. SUDDEN INFANT DEATH SYNDROME (SIDS) • ETIOLOGY: • Unknown • Hypothesis: related to brainstem abnormality in neurologic regulation of cardiorespiratory control • Abnormalities: prolonged sleep apnea, increased frequency of brief inspiratory pauses, excessive periodic breathing, impaired arousal responsiveness to increase carbon dioxide or decrease oxygen • Sleep apnea is not the cause of SIDS; genetic predisposition has been postulated as the cause • Autopsies: pulmonary edema & intrathoracic hemorrhages • Should be performed on all infants suspected of dying of SIDS
  • 153. SUDDEN INFANT DEATH SYNDROME (SIDS) • INFANTS AT RISK FOR SIDS: • Infants with 1 or more ALTEs requiring cardiopulmonary resuscitation (CPR) or vigorous stimulation • Preterm infants who continue to have apnea at the time of hospital discharge • Siblings of 2 or more SIDS victim • Infants with certain types of disease or conditions – central hypoventilation • Home monitoring and/or use of respiratory stimulant drugs recommended • No diagnostic tests exist to predict which infants will survive
  • 154. SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Educate families in prevention of SIDS • Risk of prone sleeping position in infant births – 6 months • Use of appropriate beddings, parental smoking around infant and dangers of sharing an adult bed with infant • Post partum discharge planning, newborn discharge teaching and newborn- care classes • Follow-up visits, well-baby clinic visits, immunization visits • Discuss infant sleep position
  • 155. SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Psychologic intervention – loss of child • Practices that may reduce the risk of SIDS • Avoid smoking during pregnancy and near the infant • Encouraging supine sleeping position • “back to sleep” • Avoid soft, moldable mattresses, blankets, pillows • No pillows/ quilts, stuffed toys, towels • Discouraging bed sharing • Encourage breastfeeding
  • 156. SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Avoid overheating during sleep • Infants should wear light-clothing, comfortable room temperature • Infant’s head position should be varied to prevent flattening of the skull • Use of pacifier – protective against occurrence of SIDS; naptime and bedtime, no sweetened coating • Finding the infant • it’s always the mother who finds child dead in crib • Child is in disheveled bed w/ blankets over head, huddled in 1 corner
  • 157. SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Frothy, blood-tinged fluid fills the mouth & nostrils, lying face down in secretions (bled to death) • Diaper is wet and full of stool – cataclysmic type of death • Parents must deal with his/her initial shock, panic, grief • Compassionate, sensitive approach to family
  • 158. SUDDEN INFANT DEATH SYNDROME (SIDS) • NURSING CONSIDERATIONS: • Arriving at emergency department • No attempt at resuscitation • Parents are asked only factual questions – when they found the infant, how he/she looked • No misguided statements: “this looks like suffocation” (guilt) • Discuss possible autopsy • Compassionate care – allow them to say good-bye to their child
  • 159.
  • 160. APNEA OF PREMATURITY (AOP) • Preterm infants; rare: full-term • Apneic spells increase in prevalence the younger the gestational age • 1/3 infants <33 weeks AOG, >1/2 healthy infants < 30 weeks AOG • Resolves as infant reaches 37 weeks postmenstrual age • Preterms are periodic breathers – periods of rapid respirations separated by periods of very slow breathing, often short periods with no visible or audible respirations • Apnea – extension of periodic breathing • Lapse of spontaneous breathing for 20 seconds or longer, that may or may not be followed by bradycardia, oxygen desaturation and color change • Temporary apnea - <15-20 seconds • Pathologic apnea - > 20 seconds
  • 161. APNEA OF PREMATURITY (AOP) • Classification according to origin: • Central Apnea – absence of diaphragmatic and other respiratory effort • Occurs when CNS does not transmit signals to the respiratory muscle • Obstructive Apnea – air flow ceases because of upper airway obstruction yet chest or abdominal wall movement is present • Mixed Apnea: combination of central and obstructive apnea • Most common apnea seen in preterm infants
  • 162. APNEA OF PREMATURITY (AOP) • PATHOPHYSIOLOGY: • Reflects the immature and poorly refined neurologic and chemical respiratory control mechanism in premature infants • Not responsive to hypercarbia and hypoxemia, have fewer dendritic associations than those of more mature infants • Respiratory reflexes less mature – contributing factor in etiology • Weakness of muscles of thorax, diaphragm and upper airway – contribute to apneic episodes
  • 163. APNEA OF PREMATURITY (AOP) • PATHOPHYSIOLOGY: • Apnea – observed during periods of REM sleep • Precipitated/ worsened by a variety of factors: • Infection • Intracranial hemorrhage • PDA • Secondary causes: investigated in infants with new-onset apnea or when there’s significant change in frequency or severity of apneic episodes • Apnea in full-term: consider secondary cause
  • 164. APNEA OF PREMATURITY (AOP) • POSSIBLE CAUSES OF APNEA OF PREMATURITY: • Prematurity • Airway obstruction with mucus or milk, or poor positioning • Anemia, polycythemia • Dehydration • Cooling / overheating • Hypoxemia • Hypercapnia / hypocapnia • Hypoglycemia, hypocalcemia, hyponatremia • Sepsis, meningitis • Seizures • Increased vaga tone (in response to suctioning nasopharynx, gavage tube insertion, reflux of gastric contents, endotracheal intubation) • CNS depression – pharmacologic agents • Intraventricular hemorrhage (IVH) • Patent ductus arteriosus (PDA), congestive heart failure (CHF) • Depression following maternal obstetric sedation • Respiratory distress – pnemonia, inborn errors of metabolism (hyperammonemia), congenital defects of upper airways
  • 165. APNEA OF PREMATURITY (AOP) • CLINICAL MANIFESTATIONS: • Persistent apneic spells • TREATMENT • Observe for apnea • Check for thermal stability • Administration of methylxanthines (theophylline, aminophylline or caffeine) • Reduce frequency of primary apnea-bradycardia spells in newborn • CNS stimulants to breathing • Observe for symptoms of toxicity • Caffeine – fewer side effects ; once daily dosing • Monitor weight and urine output
  • 166. APNEA OF PREMATURITY (AOP) • TREATMENT: • Nasal continuous positive airway pressure (NCPAP) and intermittent positive pressure ventilation • CPAP acts to maintain airway patency • More effective for obstructive/ mixed apnea
  • 167. APNEA OF PREMATURITY (AOP) • NURSING CONSIDERATION: • Monitor respiration and heart rate routinely in all preterm infants • Observe for presence of respirations • Observe color • Provide gentle tactile stimulation – rubbing the back/ chest gently, turning infant to supine position • If tactile stimulation fails to reinstitute respiration – flow by oxygen and suctioning of nose and mouth • Apply artificial ventilation with bag-valve mask and with sufficient pressure to lift rib cage • If breathing does not begin • Raise chin gently to open airway • Infant is never shaken
  • 168. APNEA OF PREMATURITY (AOP) • NURSING CONSIDERATION: • After breathing is restored: assess for and manage any precipitating factors (temperature instability, abdominal distention, ambient oxygen) – use pulse oximetry • Record episodes of apnea - # apneic spells, appearance during and after the episode, did infant self-recover or whether tactile stimulation or other measures were done to restore breathing. • Investigate possible cause of apneic episode • Observe for signs of theophylline or caffeine toxicity; tachycardia (rate 180-190/ min) and later, vomiting, restlessness, irritability • Assess skin (with NCPAP) for breakdown, irritation, and nasal septum
  • 169.
  • 170. AUTISTIC SPECTRUM DISORDER (AUTISM) • Complex developmental disorder of brain function accompanied by intellectual and behavioral deficits • Manifested during early childhood: 18-36 months of age • 1-2 in 500 children; males > females (females more severely affected) • Not related to socioeconomic level, race, parenting style
  • 171. AUTISTIC SPECTRUM DISORDER (AUTISM) • ETIOLOGY • Unknown • Multiple biologic causes • Abnormal EEG, epileptic seizures, delayed development of hand predominance, persistence of primitive reflexes, metabolic abnormalities (increased serotonin), hypoplasia of vermis of cerebellum • Increased in twins • High risk of recurrence of ASD in families with one affected child • Not caused by thimerosal-containing vaccines • Associated with fragile X syndrome, tuberous sclerosis, metabolic disorder, fetal rubella syndrome, H. influenza meningitis, structural brain anomalies • Perinatal events: higher incidence of maternal uterine bleeding during pregnancy • Lower incidence of maternal vaginal infections during pregnancy • Decreased maternal use of contraceptives • Higher incidence of neonatal hyperbilirubinemia
  • 172. AUTISTIC SPECTRUM DISORDER (AUTISM) • CLINICAL MANIFESTATIONS AND DIAGNOSTIC EVALUATION: • Hallmark: inability to maintain eye contact with another person • Display limited functional play and may interact with toys in an unusual manner • Deficits in social development: primary feature of illness • Majority have some degree of mental retardation • Females tend to have very low intelligence scores • Savants – children with ASD who excel in particular areas: art, music, memory, mathematics, perceptual skills (puzzle building)
  • 173. AUTISTIC SPECTRUM DISORDER (AUTISM) • Speech and language delays • Immediate evaluation of any child who does not display such language skills as babbling or gesturing by 12 months, single word by 16 months, 2-word phrases by 24 months • Sudden deterioration in extant expressive speech is also a red-flag event for further evaluation
  • 174. AUTISTIC SPECTRUM DISORDER (AUTISM) • DIAGNOSTIC CRITERIA FOR ASD: • Total of 6 (or more) items from (1), (2), (3) with at least two from (1), and one each from (2) & (3) (1) Qualitative impairment in social interaction, as manifested by at least 2 of the following: • Marked impairment in use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, & gestures to regulate social interaction • Failure to develop peer relationships appropriate to developmental level • A lack of spontaneous seeking to share enjoyment, interests, or achievements w/ other people (ex. By a lack of showing, bringing, or pointing out objects of interest) • Lack of social/ emotional reciprocity
  • 175. AUTISTIC SPECTRUM DISORDER (AUTISM) (2) Qualitative impairments in communication as manifested by at least 1 of the following: • Delay in, or total lack, of the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime) • In individuals w/ adequate speech, marked impairment in the ability to initiate or sustain a conversation with others • Stereotyped and repetitive use of language or idiosyncratic language • Lack of varied, spontaneous, make-believe play or social imitative play appropriate to developmental level
  • 176. AUTISTIC SPECTRUM DISORDER (AUTISM) (3) Restricted repetitive and stereotyped patterns of behavior, interests & activities, as manifested by at least 1 of the following: • Encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus • Apparently inflexible adherence to specific, nonfunctional routines or rituals • Stereotyped & repetitive motor mannerisms (ex. Hand or finger flapping or twisting, or complex whole- body movements) • Persistent preoccupation w/ parts of objects • Delays or abnormal functioning in at least 1 of the following areas with onset before age 3 years • Social interaction • Language as used in social communication • Symbolic or imaginative play • The disturbance is not better accounted for by Rett disorder or childhood disintegrative disorder
  • 177. AUTISTIC SPECTRUM DISORDER (AUTISM) • PROGNOSIS: • Severely disabling condition • Some improve with acquisition of language skills & communication w/ others • Some achieve independence, but most require lifelong adult supervision • Aggravation of psychiatric symptoms – ½ children during adolescence, w/ girls having tendency for continued deterioration • Most favorable for children who develop communicative speech by age, years & have an IQ higher than 50 at time of diagnosis
  • 178. AUTISTIC SPECTRUM DISORDER (AUTISM) • NURSING CARE MANAGEMENT: • No cure for ASD but there are numerous therapies • Highly structured & intensive behavior modification programs • Promote positive reinforcement, increase social awareness of others, teach verbal communication skills and decrease unacceptable behavior • Provide a structured routine for the child to follow – key management in ASD
  • 179. AUTISTIC SPECTRUM DISORDER (AUTISM) • NURSING CARE MANAGEMENT: • Hospitalized child with ASD: dcrease stimulation • Place child in private room • Avoid extraneous auditory & visual distraction • Encourage parents to bring in possessions to which child is attached • Minimum holding & eye contact • Care must be taken when performing procedures, administering meds, feeding these children – may swallow thermometer, gags when eating • Family support - counseling
  • 180.
  • 181. MAJOR STRESSORS OF HOSPITALIZATION • SEPARATION ANXIETY • Middle infancy – preschool age • STAGES: • PROTEST PHASE: • Cry and scream • Cling to parent • Avoids/ rejects contact with strangers • Verbally and physically attack strangers • Attempts to escape and find parents
  • 182. MAJOR STRESSORS OF HOSPITALIZATION • DESPAIR PHASE: • Crying stops, evidence of depression • Less active • Uninterested in food • Withdraws from others • Child’s physical condition may deteriorate from refusal to eat, drink, or move • DETACHMENT PHASE: • Denial; resignation and not contentment • Child becomes more interested in the surroundings • Forms new but superficial relationship • May have serious attachment to parent after separation
  • 183. MAJOR STRESSORS OF HOSPITALIZATION • LOSS OF CONTROL • INFANTS • Trust • Consistent, loving caregivers • Attempts to control their environment through emotional expressions • TODDLERS • Autonomy • When their egocentric pleasures meet with obstacles, they react with negativism • Results from altered routines and rituals
  • 184. MAJOR STRESSORS OF HOSPITALIZATION • PRESCHOOLERS • Suffer loss of control by physical restriction, altered routines, and enforced dependency • Egocentric and magical thinking typical of age • May view illness and hospitalization as punishment for misdeed • PREOPERATIONAL THOUGHT – explanations are understood only in terms of real events • TRANSDUCTIVE REASONING – deduct from the particular to particular, rather than from the specific to the general
  • 185. MAJOR STRESSORS OF HOSPITALIZATION • SCHOOL AGE • Striving for independence and productivity • Altered family roles, physical disability, fears of death, abandonment, permanent injury, loss of peer acceptance, lack of productivity • Boredom • ADOLESCENTS • Struggle for independence, self assertion and liberation – personal identity • Separation from peer group • May respond with anger, frustration • Voluntarily isolate themselves from age mates until they can feel they can compete • Need for information about their condition
  • 186. MAJOR STRESSORS OF HOSPITALIZATION • FEARS OF BODILY INJURY AND PAIN • Common fear among children • May persist into adulthood and result in avoidance of needed care • YOUNG INFANT’S RESPONSE TO PAIN: <6 months • Generalized response of rigidity, thrashing • Loud crying • Facial expressions of discomfort – most consistent indicator of stress • No understanding of the relationship between stimuli and subsequent pain.
  • 187. MAJOR STRESSORS OF HOSPITALIZATION • OLDER INFANT’S RESPONSE TO PAIN: (6months – 1year) • Withdrawal from painful stimuli • Loud crying • Facial grimace • Physical resistance • YOUNG CHILD’S RESPONSE TO PAIN: (toddlers) • Loud crying; screaming • Verbalization, “ow”, “ouch”, “it hurts” • Thrashing of limbs • Attempts to push away stimulus • Uncooperative; needs restraints • Clings to parent, nurse, or other significant person • Request emotional support
  • 188. MAJOR STRESSORS OF HOSPITALIZATION • SCOOL-AGE CHILD’S RESPONSE TO PAIN • Stalling behavior – “wait a minute”, “I’m not ready” • Muscle rigidity • May use all behaviors of young child • ADOLESCENT’S RESPONSE TO PAIN • Less vocal protest, less motor activity • Increased muscle tension and body control • More verbalization (“It hurts”, You’re hurting me!”)
  • 189. INDIVIDUAL RISK FACTORS THAT INCREASE VULNERABILITY TO STRESSES OF HOSPITALIZATION • “Difficult” temperament • Lack of fit between child and parent • Age (especially between 6 months and 5 years old) • Male gender • Below average intelligence • Multiple and continuing stresses (ex. Frequent hospitalizations)
  • 190. BENEFICIAL EFFECT OF HOSPITALIZATION • Recovery from illness • Increase coping skills • Master stress and feel competent in coping • New socialization experiences
  • 191. PREVENTING OR MINIMIZING SEPARATION • Primary nursing goal • Especially for children < 5 years old • Family-centered care • Parents are not “visitors” • Familiar items from home
  • 192. NORMALIZING THE HOSPITAL ENVIRONMENT • Maintain child’s routine, if possible • Time structuring • Self-care (age appropriate) • School work • Friends and visitors
  • 193. PREVENTING OR MINIMIZING FEAR OF BODILY INJURY • All children fear bodily injury from mutation, bodily intrusion, body- image change, disability, or death. • Preparation of children for painful procedures decreases their fears. • Use of bandages • Repeatedly stress the reason for a procedure • Adolescents may express concern about the actual procedure but more anxious about the resulting scar.
  • 194. PAIN FACTS AND FALLACIES • FACT: Children are under treated for pain. • FACT: Analgesia is withheld for fear of the child becoming addicted • FALLACY: Analgesia should be withheld because it may cause respiratory depression in children • FALLACY: Infants do not feel pain.
  • 195. PRINCIPLE OF PAIN ASSESSMENT IN CHILDREN: QUESTT • Question the child. • Use pain rating scale. • Evaluate behavioral & physiologic changes. • Secure parent’s involvement. • Take the cause of pain into account. • Take action and evaluate result. • Question the child – verbal & description of pain. Ask child to point where it hurts. • Use of Pain Rating Scale – provide a quantitative self-reporting measure of pain.
  • 196. PAIN RATING SCALES • Not all pain rating scale are reliable or appropriate for children • Should be age appropriate • Consistent use of same scale by all staff. • Familiarize child with scale
  • 197. PAIN RATING SCALE F.L.A.C.C (FACE, LEGS, ACTIVITY, CRY, CONSOLABILITY 0 1 2 FACE No particular expression or smile Occasional grimace or frown, withdrawn, disinterested Frequent to constant frown, clenched jaw, quivering chin LEGS ACTIVITY Normal, relaxed position, moves easily Uneasy, restless, tense, shifting back and forth Arched, rigid or jerking CRY No cry (awake or asleep) Moans, whimpers, occasional complaint Crying steadily, screams or sobs, frequent complaints CONSOLABILITY Content, relaxed Reassured by occasional touching, hugging or talking to Difficult to console or comfort
  • 198. CHILDREN’S DEVELOPMENTAL CONCEPT OF ILLNESS • PREOPERATIONAL THOUGHT (2-7years) • PHENOMENISM – perceives an external, unrelated, concrete phenomenon as cause of illness • CONTAGION – perceives cause of illness as proximity between 2 events that occur by magic
  • 199. CHILDREN’S DEVELOPMENTAL CONCEPT OF ILLNESS • CONCRETE OPERATIONAL THOUGHT (7-10years) • CONTAMINATION – perceives cause as a person, object, or action external to the child that is “bad” or “harmful” to the body • INTERNALIZATION – perceives illness as having an external cause but as being located inside the body
  • 200. CHILDREN’S DEVELOPMENTAL CONCEPT OF ILLNESS • FORMAL OPERATIONAL THOUGHT (13yrs & above) • PHYSIOLOGIC – perceives cause as malfunctioning or nonfunctioning organ or process; can explain illness in sequence of events • PSYCHOPHYSIOLOGIC – realizes that psychologic actions and attitudes affect health and illness.