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Chapter 14The Newborn with a Perinatal Injury or Congenital MalformationBirth DefectsAbnormalities that are apparent at birthThe abnormality may be of StructureFunctionMetabolismMay result in a physical or mental disability, may shorten life, or may be fatalClassifications of Birth DefectsMalformations present at birthMay also be known as congenital malformationsInborn errors of metabolismDisorders of the bloodChromosomal abnormalitiesPerinatal injuriesMarch of DimesBirth defects cannot be attributed to a single cause. Combination of environment and heredityInherited susceptibilityStage of pregnancyDegree of environmental hazardNervous SystemNeural tube defectsMost often caused by failure of neural tube to close at either the cranial or the caudal end of the spinal cordHydrocephalusSpina bifidaHydrocephalusCharacterized by an increase in CSF within the ventricles of the brainCauses pressure changes in the brainIncrease in head sizeResults from an imbalance between production and absorption of CSF or improper formation of ventriclesHydrocephalus (cont.)Most commonly acquired byAn obstruction A sequelae of infectionPerinatal hemorrhageSymptoms depend onSite of obstructionAge at which it developsHydrocephalus (cont.)ClassificationsNoncommunicatingObstruction of CSF flow from the ventricles of the brain to the subarachnoid spaceCommunicating CSF is not obstructed in the ventricles but is inadequately reabsorbed in the subarachnoid spaceManifestations of HydrocephalusDepends on time of onset and severity of imbalanceClassic signsIncrease in size of headCranial sutures separate to accommodate enlarging massScalp is shinyVeins are dilatedDiagnosis and Treatment of HydrocephalusDiagnosisTransilluminationEchoencephalographyCT scanMRIVentricular tap or punctureTreatmentMedications to reduce production of CSFSurgery to place a shuntSymptoms of Increasing Intracranial PressureIncreased blood pressureDecrease in pulse rateDecrease in respirationsHigh-pitched cryUnequal pupil size or response to lightBulging fontanels in infantsHeadaches in children due to closed cranial suturesIrritability or lethargyVomitingPoor feedingVentriculoperitoneal ShuntTreatmentMedications to reduce CSF productionSurgeryShunt acts as a focal spot for infection and may need to be removed if infections persistPreoperative and Postoperative Nursing CarePre-OpFrequent head position changes to prevent skin breakdown, head must be supportedHead must be supported at all times while being fedMeasure head circumference along with other vital signsPost-OpAssess for signs of increased intracranial pressureProtect from infectionDepress shunt “pump” as ordered by surgeonPosition dependent upon multiple factorsAssess and provide for pain controlParent EducationTeach signs that indicate shunt malfunction may be occurringHow to “pump” the shuntSigns of shunt malfunction in the older child can includeHeadacheLethargyChanges in LOCSpina Bifida (Myelodysplasia)Spina Bifida (Myelodysplasia) (cont.)Group of CNS disorders characterized by malformation of the spinal cordA congenital embryonic neural tube defect with an imperfect closure of the spinal vertebraeTwo typesOcculta (hidden)Cystica (sac or cyst)Spina Bifida OccultaMinor variation of the disorderOpening is smallNo associated protrusion of structuresOften undetectedMay have a tuft of hair, dimple, lipoma, or discoloration at the siteSpina Bifida Occulta (cont.)Treatment generally not necessary unless neuromuscular symptoms appear, such asProgressive disturbances of gaitFoot dropDisturbances of bowel and bladder sphincter functionSpina Bifida CysticaDevelopment of a cystic mass in the midline of the opening in the spineMeningoceleContains portions of the membranes and CSFSize variesMeningomyelocele More serious protrusion of membranes and spinal cord through the openingMay have associated paralysis of lower extremitiesMay have poor or no control of bladder or bowelHydrocephalus is a common complicationPrevention of Spina Bifida Mother takes folic acid 0.4 mg per day prior to becoming pregnant and/or continues to take the folic acid supplement until the 12th week of pregnancyTreatment of Spina Bifida Surgical closurePrognosis is dependent upon extent of spinal cord involvementMeningoceleContains portions of the membranes and CSFIf no weakness of the legs or sphincter involvement, surgical correction is performed with excellent resultsMeningomyelocele Protrusion of the membranes and spinal cord through the openingSurgical intervention is done for cosmetic reasons and to help prevent infectionHabilitation is usually necessary post-op because the legs remain paralyzed and the patient is incontinent of urine and fecesHabilitationPatient is disabled from birthAim is to minimize the child’s disabilityConstructively use all unaffected parts of the bodyEvery effort is made to help the child develop a healthy personality so that he or she may experience a happy and productive lifeNursing Care of Spina BifidaPrevent infection of, or injury to, the sacCorrect positioning to prevent pressure on sacPrevent development of contracturesGood skin careAdequate nutritionAccurate observations and chartingEducation of the parentsContinued medical supervision and habilitationNursing Care of Spina Bifida (cont.)Upon delivery, the newborn is placed in an incubatorMoist, sterile dressing of saline or an antibiotic solution may be ordered to prevent drying of the sacProtection from injury and maintenance of a sterile environment for the open lesion are essentialNursing Care of Spina Bifida (cont.)Size and area of sac are checked for any tears or leakageExtremities are observed for deformities and movementHead circumference is measuredFontanels are observed to provide a baseline for future assessmentsNursing Care of Spina Bifida (cont.)Complications that can be life-threatening must be monitoredMeningitisPneumoniaUTIUrological monitoringSkin careFeedingPotential for latex allergy Gastrointestinal SystemCleft LipCharacterized by a fissure or opening in the upper lipFailure of maxillary and median nasal processes to unite during embryonic developmentMany cases are hereditary, others are environmentalAppears to occur more often in boys than girlsTreatmentInitial repair of cleft lip is known as cheiloplastyRepair by 3 months of ageInfant may have to have elbow restraints to prevent the infant from scratching the lipA special syringe or bottle may be needed to assist in feeding the child until surgery has occurredPostoperative Nursing CarePrevent infant from sucking and cryingCareful positioning to avoid injury to operative sitePreventing infection and scarring by gentle cleansing of suture lines to prevent crusts from formingProviding for the infant’s emotional needs by cuddling and other forms of affectionProviding appropriate pain relief measuresFeedingFed by medicine dropper until wound is completely healed (about 1 to 2 weeks)Cleanse the mouth by giving the infant small amounts of sterile water at the end of each feeding sessionCleft PalateThe failure of the hard palates to fuse at the midline during the 7th to 12th weeks of gestationForms a passageway between the nasopharynx and the noseIncreases risk of infections of the respiratory tract and middle earsCleft Palate TreatmentGoals of therapyUnion of the cleftImproved feedingImproved speechImproved dental developmentThe nurturing of a positive self-imageMultidisciplinary Team CareAlong with the patient and familyPsychologistSpeech therapistPediatric dentistOrthodontistSocial workerPediatrician Other FactorsPsychosocial adjustment of the familyFollow-up careHome careSurgery between 1 year and 18 months of agePostoperative Treatment and Nursing CareNutritionDiet is progressively advancedNo food through straws to prevent suckingOral hygieneFollow each feeding with clear water to cleanse the mouthSpeechEncourage children to pronounce words correctlyDiversionCrying should be avoided whenever possible; play should be of the quiet type (e.g., coloring, drawing, reading to the child)ComplicationsEar infections and tooth decayMusculoskeletal SystemClubfootMost common deformities Congenital anomalyFoot twists inward or outwardTalipes equinovarus is the most common typeFeet turned inwardChild walks on toes and outer borders of feetGenerally involves both feetClubfoot (cont.)Treatment and Nursing CareStarted as soon as possible or bones and muscles will continue to develop in an abnormal mannerConservative treatmentSplinting or casting to hold foot in correct positionPassive stretching exercisesIf not effective after about 3 months, surgical intervention may be indicatedParent EducationStress importance of complying with physician orders to prevent skin breakdown and possible isolation of the older child The nurse should review with the parentsCast careEmotional supportDevelopmental Hip DysplasiaDevelopmental Hip Dysplasia (cont.)Hip dysplasia applies to various degrees of deformities, subluxation or dislocation (can be partial or complete)Head of femur is partly or completely displacedSeven times more common in girlsMore apparent as infant/toddler begins walkingDevelopmental Hip Dysplasia (cont.)Usually discovered at routine health checks during the first or second month of lifeMost reliable sign is limited abduction of the leg on the affected sideDiagnostics for Hip DysplasiaBarlow’s test: upon adduction and extension of the hips (with health care provider providing stabilization to the pelvis), may “feel” the dislocation actually occurOrtolani’s sign (or click): health care provider can actually feel and hear the femoral head slip back into the acetabulum under gentle pressureTreatment of Hip DysplasiaHips are maintained in constant flexion and abduction for 4 to 8 weeksKeeps head of femur within the hip socketConstant pressure enlarges and deepens acetabulumCan use a Pavlik harness to provide the necessary positioningSurgical intervention may be necessaryPavlik Harness, Body Cast, and Traction Nursing Care of Infant/Child in a Spica CastNeurovascular assessment of affected extremitiesPlace firm, plastic-covered pillows beneath the curves of the cast for supportIn the older child, a “fracture” bedpan should be readily available for toiletingHead of bed slightly elevated to help drain any body fluids away from castFrequent changes of position are needed to prevent skin breakdownNursing Care of Infant/Child in a Spica Cast (cont.)Toys that are small enough to “hide” in the cast should not be given to the childImportant to meet everyday needsA special wagon with pillows inside it for support is one of the safest ways to transport a child in a spica castMetabolic DefectsInborn errors of metabolism involve a genetic defect that may not be apparent until after birthSymptoms to report would includeLethargyPoor feedingHypotoniaUnique odor to body or urineTachypneaVomitingPhenylketonuria (PKU)Faulty metabolism of phenylalanine, an amino acid essential to life and found in all protein foodsInfant unable to digest this essential acid and phenylalanine accumulates in blood and is found in the urine within the first week of lifeResults in severe mental retardation if not caught early Phenylketonuria (PKU) (cont.)Appears normal at birthBy the time urine test is positive, brain damage has already occurredDelayed development apparent at 4-6 monthsMay have failure to thrive, eczema, or other skin conditionsChild has a musty odorPersonality disorderOccurs mainly in blonde, blue-eyed childrenResults from a lack of tyrosine (needed for melanin formation)PKU DiagnosticsGuthrie testBlood for this test should be obtained 48 to 72 hours after birthPreferably after the infant has ingested proteinsMany states require this test to be performed prior to discharge from hospitalPKU TreatmentClose dietary managementFrequent evaluation of blood phenylalanine levelSynthetic food that provides enough protein for growth and tissue repairSpecial formulas are availableInfants: Lofenalac or Phenex-1Children: Phenyl-freeAdolescents: Phenex-2PKU Nursing CareTeach parents importance of reading food labelsFollowing up as required with health care provider for blood testsReferral to a dietitian is helpful in providing parental guidance and supportGenetic counseling may also be indicatedHealth PromotionChildren with PKU must avoid the sweetener aspartame (NutraSweet) because it is converted to phenylalanine in the bodyMaple Syrup Urine DiseaseDefect in the metabolism of branched-chain amino acidsCauses marked serum elevations of leucine, isoleucine, and valineResults in acidosis, cerebral degeneration, and death within 2 weeks if not treatedMaple Syrup Urine Disease (cont.)Appears healthy at birth, but problems soon developFeeding difficultiesLoss of the Moro reflexHypotonia Irregular respirationsConvulsions Maple Syrup Urine Disease (cont.)ManifestationsUrine, sweat, and cerumen (earwax) have a characteristic maple syrup odor caused by ketoacidosisDiagnosis confirmed by blood and urine testsMaple Syrup Urine Disease Treatment and Nursing CareTreatmentRemoving the amino acids and their metabolites from the body tissuesHydration and peritoneal dialysis to decrease serum levelsLifelong diet low in amino acids leucine, isoleucine, and valineExacerbations are usually related to degree of abnormality of leucine levelInfection can be life-threateningGalactosemiaUnable to use galactose and lactoseEnzyme needed to help the liver convert galactose to glucose is defective or missingResults in an increased serum galactose level (galactosemia) and in the urine (galactosuria)If untreated can causeCirrhosis of the liverCataractsMental retardationGalactose is present in milk in the form of sugar; therefore, early diagnosis is essentialGalactosemia (cont.)Begins abruptly, worsens graduallyEarly signsLethargyVomitingHypotoniaDiarrheaFailure to thriveSymptoms begin as the newborn is fedJaundice may be presentGalactosemia Treatment and Nursing CareMilk and lactose-containing products are eliminated from the dietBreastfeeding must be stoppedLactose-free formulas or soy protein–based formulas are often used insteadParental support and education is essentialChromosomal AbnormalitiesDown SyndromeMost common chromosomal abnormalityRisk increases with Mothers 35 years and olderFathers 55 years and olderInfant has mild to severe mental retardationSome physical abnormalities are also seenDown Syndrome (cont.)Three phenotypesTrisomy 21Most commonThere are three number 21 chromosomes instead of the usual twoResults from nondisjunction (failure to separate)MosaicismOccurs when both normal and abnormal cells are presentTend to be less severely affected in appearance and intelligenceTranslocation of a chromosomeA piece of chromosome in pair 21 breaks away and attaches itself to another chromosomeDown Syndrome (cont.)Screening for this is offered during prenatal care starting around week 15 of gestationAllows parents the opportunity to decide on whether to continue or terminate the pregnancy“Quad Test”: Alpha-fetoprotein (AFP), hCG, unconjugated estriol, inhibin-A levels are used for diagnosisAmniocentesis is most accurate Down Syndrome ManifestationsDown Syndrome Manifestations (cont.)Limp, flaccid posture caused by hypotonicity of musclesMore difficult to position and holdContributes to heat lossProne to respiratory illnesses and constipation due to the hypotonicityIncidence of acute leukemia is higherAlzheimer’s disease more common to those who reach middle adult lifeEncourage parents to express their feelings and concernsProvide parents with support and community referralsDevelopmental MilestonesSittingRolling overSitting aloneCrawlingCreepingStandingWalkingTalkingSelf-Help SkillsEatingToilet trainingDressingPerinatal InjuriesHemolytic Disease of the Newborn (Erythroblastosis Fetalis)Becomes apparent in utero or soon after birthRh-negative mother and Rh-positive father produce Rh-positive fetusEven though maternal and fetal blood do not mix during pregnancy, small leaks may allow fetal blood to enter the maternal circulation causing the mother’s body to start producing antibodies that cross the placenta and destroy the blood cells of the fetus, which can cause anemia and heart failure in the developing/growing fetusErythroblastosis Fetalis: Maternal SensitizationErythroblastosis Fetalis: Maternal Sensitization (cont.)Mother accumulates antibodies with each pregnancyChance of complications occurs with each subsequent pregnancySevere form, hydrops fetalis, progressive hemolysis causes anemia, heart failure, fetal hypoxia, and anasarcaErythroblastosis Fetalis Diagnosis and PreventionMaternal health history that includesPrevious Rh sensitizationsEctopic pregnancyAbortionBlood transfusionsChild who developed jaundice or anemia during a neonatal periodIndirect Coombs’ test will indicate previous exposure to Rh-positive antigensErythroblastosis Fetalis Diagnosis and Prevention (cont.)Confirmed by amniocentesis and monitoring of bilirubin levels in the amniotic fluidFetal Rh status can be determined non-invasively via free DNA in maternal plasmaDiagnostic studies will help the physician to determine if early interventions, such as induction of labor or intrauterine fetal transfusions, are neededErythroblastosis Fetalis Diagnosis and Prevention (cont.)Use of Rh(D) immune globulin (RhoGAM)Administered within 72 hours of delivery with an infant who is Rh-positive, an ectopic pregnancy, or after an abortionMay also be given to the pregnant woman at 28 weeks gestationErythroblastosis Fetalis ManifestationsDirect Coombs’ test on umbilical cord bloodSymptoms vary Anemia caused by hemolysis of large numbers of erythrocytesPathological jaundice occurs within 24 hours of delivery; liver cannot handle the amount of hemolysis, bilirubin levels rise rapidlyEnlargement and edema of liver and spleenOxygen-carrying capacity of the blood is diminished, including blood volumeInfant at major risk of shock or heart failureErythroblastosis Fetalis Manifestations (cont.)Kernicterus—bilirubin has reached toxic levelsAccumulated bilirubin in the brain tissue can cause serious brain damage and permanent disabilityInfant will have jaundice along withIrritabilityLethargyPoor feedingHigh-pitched, shrill cryMuscle weaknessProgresses to opisthotonosSeizuresErythroblastosis Fetalis Treatment Prompt identificationLaboratory testsDrug therapyPhototherapyExchange transfusions, if indicatedErythroblastosis Fetalis Nursing CareEnsure eyes are protected from phototherapyCover gonadsProvide incubator careCentral line care (usually the umbilical vein)Observe newborn’s colorApply wet, sterile compresses to the umbilicus, if ordered, until transfusions are completeNursing Tip Assessing jaundice involves The skin and the whites of the eyes assume a yellow-orange castBlanching the skin over bony prominences enhances the evaluation of jaundiceJaundice that occurs on the first day of life is always pathological and requires prompt interventionHome PhototherapyUsed for newborns with mild to moderate physiological (normal) jaundiceLess costlyMay decrease the need for hospitalizationIntracranial HemorrhageMost common type of birth injuryMay result from trauma or anoxiaOccurs more often in preterm infantsMay also occur during precipitate delivery or prolonged laborSigns and symptoms vary depending on severityIntracranial Hemorrhage (cont.)Diagnosis History of traumatic deliveryCT or MRI scanEvidence of an increase in CSF pressureTreatmentOxygenGentle handlingElevated headMedications may be prescribedCare with feeding because sucking reflex may be affectedIntracranial Hemorrhage (cont.)If convulsion occurs, notify physician immediatelyBe ready to answer the following questionsWere the arms, legs, or face involved?Was the right or left side of the body involved? Was the convulsion mild or severe?How long did it last?What was condition of infant before and after the seizure (i.e., vital signs, skin color)?Transient Tachypnea of the Newborn (TTN)Characterized byTachypneaMay also includeChest retractionsGruntingMild cyanosisOften referred to as respiratory distress syndrome, type IITypically resolves suddenly after 3 daysMay be caused by slow absorption of fluid in lungs after birthSupportive nursing and medical careMeconium Aspiration SyndromeIn uteroFetus expels meconium into amniotic fluidCord compression or other condition interrupts fetal circulationIf asphyxia or acidosis occurs, fetus may have gasping movements that cause meconium-stained amniotic fluid to be drawn into the lungsAt deliveryCan occur if newborn inhales before nose and mouth have been suctionedMeconium Aspiration Syndrome (cont.)SymptomsRespiratory distressNasal flaringRetractionsCyanosisGruntingRales and rhonchiTachypnea may persist for several weeksTreatmentWarmthOxygenSupportive careNICUNeonatal Abstinence Syndrome (NAS)Caused by fetal exposure to drugs in uteroMany illicit drugs cross the placental barrier; therefore, an infant born to a woman who is an addict will suffer drug withdrawal after birthInfant may also have long-term developmental and neurological deficitsNeonatal Abstinence Syndrome (NAS) (cont.)SymptomsBody tremors and hyperirritability (primary sign)WakefulnessDiarrheaPoor feedingSneezingYawning TestingMeconium may be more accurate than neonatal urine testing for presence of drugsTreatmentSwaddlingQuiet environmentObserve for seizuresPhenobarbital Infant of Diabetic MotherLarge amounts of glucose are transferred to fetusCauses fetus to become hyperglycemicFetal pancreas produces large amount of fetal insulinLeads to hyperinsulinism, along with excess production of protein and fatty acids, often results in an LGA newborn weighing 9 pounds (4082 g) or more (macrosomia)Infant of Diabetic Mother (cont.)After delivery, infant may have low blood glucose levels and Cushingoid appearance or look healthyMay have developmental deficits and suffer complications of RDSSuffers from HypoglycemiaHypocalcemiaHyperbilirubinemiaInfant of Diabetic Mother (cont.)MonitorGlucose levelsVital signsSigns of irritabilityTremorsRespiratory distressGlucose levels below 40 mg/dL can result in rapid and permanent brain damageQuestion for ReviewHow can prenatal care prevent neural tube defects? ................
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