Diseases-and-Problems-in-the-Newborn.pdf

Diseases and Problems in the Newborn Paula Michelle M. Perez, MD Department of Pediatrics 1  Objectives Discuss high-risk pregnancies and high-risk infants Discuss the etiologies, clinical manifestations, laboratory and ancillary d...

Diseases and Problems in the Newborn Paula Michelle M. Perez, MD Department of Pediatrics 1  Objectives Discuss high-risk pregnancies and high-risk infants Discuss the etiologies, clinical manifestations, laboratory and ancillary diagnostic procedures, treatments and prognosis of common diseases and problems in the newborns 2  Neonatal Period Period between birth until 28th day of life Further subdivided into: – Very early – Early – Late neonatal period Mortality is highest during the 1st 24 hours after birth Major causes of neonatal mortality: – Prematurity – Low birth weight – Congenital anomalies 3  Neonatal Mortality Rate Defined as the total number of neonatal deaths in a year divided by the number of live births in that same year Neonatal deaths comprise 37% of all deaths occurring in children under 5 y/o 4  Review A healthy newborn is likely to come from a healthy pregnancy. First visit must be done in the _____ first trimester. At least ___ 4 prenatal visits all throughout the course of pregnancy. ____ Two doses of tetanus toxoid immunization. 5  High-Risk Pregnancy Increase the likelihood of poor outcome during pregnancy, delivery and postneonatal period. 10-20% of pregnant women can be identified as being high-risk Factors associated with High-Risk Pregnancy 1. Genetic Factors 2. Maternal Factors 6  1. Genetic Factors Occurrence of chromosomal abnormalities, congenital anomalies, inborn errors of metabolism, mental retardation or any familial diseases Specific injury should be made about any disease affecting 1 or more blood relatives 7  2. Maternal Factors Age for least risk for neonatal mortality: 20 – 30 years old Maternal illness Multiple pregnancies Infections Certain drugs In vitro fertilization Preterm birth – PROM, cervical shortening, infection Polyhydramnios, oligohydramnios 8  Review Polyhydramnios indicates amniotic fluid of 2, 000 ml during the third trimester, while >_______ oligohydramnios has a volume of 500 ml. < ____ The most serious complication of chronic pulmonary hypoplasia oligohydramnios is _____________________. 9  High-Risk Infant Infants who should be under close observation to decrease neonatal morbidity and mortality Approximately 10-20% of births 1. Multiple Gestation Pregnancies 2. Prematurity 3. Small for Gestational Age (SGA) and Intrauterine Growth Restriction (IUGR) 4. Post-Term Infants 5. Large for Gestational Age (LGA) 10 High-Risk Infant 11  High-Risk Infant Examine the placenta, cord and membrane – Fetal blood loss – placental pallor, retroplacental hematoma, tears in velamentous cords – Placental edema – hydrops fetalis, congenital nephrosis or hepatic disease – Small whitish nodules on the cord – candidal infection – Single umbilical arteries – congenital renal abnormalities, syndromes In general, for any given age, the lower the birth weight, the higher the risk of death; for any given birth weight, the shorter the gestational age, the greater likelihood of neonatal death 12  1. Multiple Gestation Pregnancies Noted with increasing incidence due to reproductive technology 3 – 5 % incidence Can be detected as early as 12 weeks age of gestation (AOG) Dizygotic – fertilization of 2 separate ova during a single cycle Monozygotic – single fertilized ovum that subsequently divides into 2 separate individuals Monozygotic twins have increased risk of IUGR, twin- twin transfusion, and congenital anomalies 13 1. Multiple Gestation Pregnancies 14  1. Multiple Gestation Pregnancies Fetal Transfusion Syndrome – Due to acute or chronic drainage of 1 twin’s artery to the vein of the other – 1 twin is large and plethoric while the other twin is anemic and small Complications of multiple gestation – Cord entanglement – Congenital anomalies – IUGR, SGA Perinatal mortality is higher in twins, especially monochorionic twins. For multiple gestations exceeding 2 fetuses, risks are increasingly higher. Anticipation of multiple pregnancies is the key. 15  Review Ballard Scoring is used in the Delivery Room _________ to assess the gestational age of the neonate. Preterm infants are those born less than ____ 37 weeks of gestation Plotting the birth weight of the neonate in the Lubchenco Chart ___________________ is used to determine the appropriateness of the birth weight with the gestational age. 16  2. Prematurity Infants born less than 37 weeks of gestation Classification Based on Birth Weight Low Birth Weight (LBW) 1, 500 – 2, 500 grams Very Low Birth Weight (VLBW) 5mg/dL/day not >5mg/dL/day TB peaks at 14-15 mg/dL TB increases to >15 mg/dL Direct Bilirubin (DB) 10% of TB TB Resolves in 1 week (term), 2 Persists beyond 1 week (term), weeks (preterm) 2 weeks (preterm) 82 83  Neonatal Hyperbilirubinemia 3 main mechanisms – Shorter lifespan of erythrocytes at 70 – 90 days – Low number of bacteria in neonatal intestine and decreased activity of beta-glucoronidase – Decreased activity of ligandin 84  Neonatal Hyperbilirubinemia Clinical Manifestations – Cephalocaudal progression – Indirect bilirubin – bright yellow or orange – Direct – greenish or muddy yellow cast – Kernicterus – lethargy, poor feeding 85  Clinical Jaundice Measure serum bilirubin Total Bilirubin ≤12 Total Bilirubin ≥12 mg/dl and neonate mg/dl and neonate Direct Bilirubin >24 HOL 2 mg/dL Decreased >2 mg/dL Common Uncommon Hyperalimentati Hepatic on cholestasis infarction TORCH infection Inborn errors of metabolism Inspissated bile Cystic fibrosis from prolonged hemolysis Neonatal Biliary atresia hepatitis Sepsis Choledochal cyst 88  Kernicterus Bilirubin encephalopathy Deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei >20mg/dL The more immature the infant is, the greater the susceptibility to kernicterus 89  Kernicterus Clinical Manifestations Term – 2 – 5 days; Preterms – 7 days Subtle early signs Initial signs: lethargy, poor feeding, loss of Moro reflex Opisthotonos with bulging fontanel Shrill, high-pitched cry Convulsions and spasm 90 Kernicterus 91  Kernicterus Prevention Practical, system-based approach Recommendations – Evaluate jaundice 35 weeks AOG for treatment of hyperbilirubinemia 93 94 95  Neonatal Hyperbilirubinemia Complications – Loose stools, erythematous macular rash, dehydration, hypothermia – Bronze Baby Syndrome – dark – grayish brown skin discoloration 96  Neonatal Hyperbilirubinemia Exchange transfusion – double volume exchange transfusion (DVET), partially remove hemolyzed and anti-body coated RBCs and replace with donor RBCs Indications for exchange transfusion – Failure of phototherapy – Continued hemolysis – Kernicterus 97  Neonatal Hyperbilirubinemia For direct hyperbilirubinemia, Phototherapy and exchange transfusion is not indicated Ursodeoxycholic acid (UDCA) is the drug of choice Surgical procedure Treat infection 98 Necrotizing Enterocolitis (NEC) Most common life-threatening emergency of the GI tract in the newborn period Multifactorial cause Pathologic findings – Necrotic segment of intestine – Pneumatosis intestinalis – gas in submucosal wall – Progression to perforation, peritonitis, sepsis 99 Necrotizing Enterocolitis (NEC) Distal part of ileum and proximal segment of colon Triad – Injury – intestinal ischemia – Metabolic substrate – enteral nutrition – Bacterial translocation Prematurity as greatest risk factor Characteristic histologic finding: Coagulation necrosis 100 Necrotizing Enterocolitis (NEC) Clinical Manifestation – onset usually in the 2nd – 3rd week of life – Age of onset inversely related to gestational age 101 Necrotizing Enterocolitis (NEC) Diagnosis – High index of suspicion – Plain abdominal radiographs: pneumatosis intestinalis (diagnostic), portal venous gas, pneumoperitoneum 102 Necrotizing Enterocolitis (NEC) 103 Necrotizing Enterocolitis (NEC) Treatment Prevent further injury; NPO, nasogastric decompression Systemic broad spectrum antibiotics Parenteral fluids Supportive care 104 Necrotizing Enterocolitis (NEC) Treatment Indications for surgery – Perforation on abdominal xray – Positive result of abdominal paracentesis – Failure of medical management Mortality in 30 – 40% of severe cases 105 HEMATOLOGIC DISORDERS 106  Anemia in the Newborn Infant Physiologic anemia – Term: 8 – 12 weeks (Hgb 11 g/dL) – Preterm: 6 weeks (7 – 10 g/dL) Anemia of prematurity – LBW 1- 3 months after birth – Hgb 2 weeks, due to Vitamin K malabsorption Breastmilk – poor source of Vitamin K 116 Hemorrhagic Disease of the Newborn 117  Hemorrhagic Disease of the Newborn Prevention: Vitamin K 1 mg IM at birth Treatment – Vitamin K 1 – 5 mg IV infusion – Blood transfusion of Fresh Frozen Plasma or whole blood 118 NERVOUS SYSTEM DISORDERS 119  Neonatal Seizures Classified according to the most prominent component – Subtle – Focal clonic – Multifocal clonic – Focal or generalized tonic – Myoclonic – Spasm – Tonic - clonic 120  Neonatal Seizures May be post-asphyxial, hemorrhagic, metabolic, toxic, infectious and genetic Benign jitteriness – Rapid, tremuluos movement of short – duration – Triggered by sensory stimulus – Abates with restraint or repositioning of the infant Diagnosis: Careful prental, perinatal and family history, complete PE and neurologic exam 121  Hypoxic – Ischemic Encephalopathy (HIE) Caused by hypoxia and ischemia to the CNS, which frequently occurs perinatally Important cause of permanent CNS damage Maybe due to different factors – Inadequate oxygenation – Low maternal blood pressure – Placental insufficiency – Abruptio placenta – Cord prolapse 122  Hypoxic – Ischemic Encephalopathy (HIE) Clinical Manifestations Severity would depend on the duration and timing of injury At birth, depressed neonates with no spontaneous respiration Pallor, cyanosis, apnea Cerebral edema may develop during the next 24 hours Systemic organ dysfunction in up to 80% of affected neonates 123 Hypoxic – Ischemic Encephalopathy (HIE) 124 Hypoxic – Ischemic Encephalopathy (HIE) 125  Hypoxic – Ischemic Encephalopathy (HIE) Diagnosis – Diffusion – weighted MRI – preferred imaging modality – Cranial Ultrasonography – in preterm Treatment – Establish and maintain adequate ventilation and perfusion – Treat and control seizures – Amplitute integrated EEG (aEEG) to prognosticate brain injury – Systemic or selective cerebral hypothermia 126  Intracranial Hemorrhage May be caused by trauma or asphyxia; rarely by primary hemorrhagic disturbance or congenital vascular anomaly Intraventricular hemorrhage (IVH) on preterm infants – Risk is inversely related to gestational age and birth weight – Predisposing factors: Prematurity, RDS, Hypoxic – ischemic or hypotensive injury, reperfusion injury of damaged vessels, abnormal cerebral blood flow 127  Intracranial Hemorrhage Periventricular Leukomalacia (PVL) – Neonates < 1,000 grams – Focal necrotic lesion un the periventricular white matter – Increased occurrence with neonates with severe IVH Clinical Manifestations – Majority have no initial clinical signs – Acute deterioration in 2nd – 3rd DOL – Pallor, cyanosis, poor suck, seizures, shock, decreased muscle tone 128  Intracranial Hemorrhage Clinical Manifestation – PVL is clinically asymptomatic and becomes apparent in later infancy as spastic deficits Diagnosis – History + Clinical Manifestations – Cranial UTZ – preferred imaging technique – All at-risk infants should undergo follow-up ultrasonography 129  Intracranial Hemorrhage Grade Severity of Hemorrhage in Cranial Imaging Grade I Bleeding isolated in subependymal area Grade II Bleeding within the ventricle, without ventricular dilation Grade III IVH + ventricular dilation Grade IV IVH + parenchymal hemorrhage Ventriculomegaly - Mild 0.5 – 1.0 cm dilated - Moderate 1.0 – 1.5 cm - evere >1.5 cm 130  Intracranial Hemorrhage ~3 – 5% of VLBW develop Posthemorrhagic Hydrocephalus (PHH), sometimes requiring ventriculoperitoneal (VP) shunt Degree of IVH and PVL strongly linked to neurodevelopmental impairment Treatment – Treat and control seizures – Correct anemia and coagulopathy – Supportive care 131  Intracranial Hemorrhage Prevention – Improved perinatal care and decrease risk for preterm delivery – Antenatal corticosteroids at 24 – 34 weeks for mothers at risk for preterm delivery 132  Review Maternal folic acid supplementation at dose of 0.4 mg once a day is recommended to reduce _________________ the incidence of Neural Tube Defects (NTD). If NTD was noted on previous pregnancy, the dose of Folic Acid should be given at 4 gms once a day ________________ ideally 1 month preconception. 133  Neural Tube Defects Failure of the neural tube to close spontaneously between 3rd – 4th week AOG 134  Neural Tube Defects Spina Bifida Occulta Occult spinal dysraphism Midline spinal defect without protrusion of spinal cord or meninges Asymptomatic patients Cutaneous manifestations: hemangioma, discoloration of the skin, pit, lump, dermal sinus, hairy patch 135  Neural Tube Defects Spina Bifida Occulta 136  Neural Tube Defects Spina Bifida Occulta Diagnosis – UTZ – initial screening – MRI – more accurate 137  Neural Tube Defects Meningocoele Meninges herniate through a defect in posterior vertebral arches or anterior sacrum Spinal cord usually normal Fluctuant midline mass that might transilluminate Thorough diagnostics before surgical procedure 138  Neural Tube Defects Myelomeningocoele Represents most severe form of dysraphism Herniation of spinal cord and meninges through a defect un the bony spinal canal Clinical Manifestations – Dysfunction of many organs and structures – Most common: Lumbosacral region 139  Neural Tube Defects Myelomeningocoele Clinical Manifestations – Low sacral region: bowel and bladder incontinence – Increased neurologic deficit as the defect extends higher into the thoracic region – Consider possibility of hydrocephalus no matter the spinal level 140  Neural Tube Defects Myelomeningocoele 141  Neural Tube Defects Myelomeningocoele Treatment – Multidisciplinary approach – Evaluate and address other congenital anomalies – Surgical procedure Prognosis – Renal dysfunction as most important determinants of mortality 142  Neural Tube Defects Anencephaly Large defect of the calvarium, meninges and scalp Rudimentary brain Absent cerebrum and cerebellum Infants die within several days after birth 143  Microcephaly Head circumference 3 SD below the mean for age and sex Main groups: Primary and Secondary Diagnosis – Serial head circumference measurement – MRI – identify structural abnormalities – TORCH assay Treatment – Provide accurate family counseling – Refer to subspecialist 144  Hydrocephalus Abnormal accumulation of cerebrospinal fluid (CSF) within the ventricular system Communicating or noncommunicating 145  Hydrocephalus Clinical Manifestations – Depends on many factors – Age – Nature of lesion – Duration and increase of intracranial pressure Treatment – Identify cause – Determine extent and associated lesions – VP Shunting – Planning for long-term follow-ups 146 NEONATAL INFECTIONS 147  Neonatal Infections Important cause of neonatal morbidity and mortality Unique due to: – Diverse modes of transmission – Immunologic immaturity – Coexisting conditions – Varying clinical manifestations – Wide variety of agents 148  Modes of Transmission 1. Intrauterine – Either transplacental route (horizontal transmission) or transcervical (ascending transmission) 2. Intrapartum 3. Post-natal 149  1. Intrauterine Infection Transplacental Infection Result of clinical or subclinical maternal infection Timing of infection affects the outcome 150  1. Intrauterine Infection Transcervical Infection Membranes rupture and infant passes through the birth canal Chroioamnionitis – Microbial invasion of amniotic fluid from prolonged rupture of membranes – Maternal fever ± signs of chorioamnionitis – Directly related to duration of rupture of membranes – 18 hours - cutoff 151 1. Intrauterine Infection 152  3. Post - Natal From exposure in the nursery or to the community (including family) Hospitalized newborns: Hand contamination 153  Early – vs Late – Onset Neonatal Infections Early – onset – acquired before or during delivery Late – onset – after delivery; from hospital or community Age at onset depends on timing of exposure and virulence of infecting organism 154  Localized Neonatal Infections Oral Thrush Oral Pseudomembranous candidiasis Candida albicans White patches inside the cheeks and tongue Tx: Oral Nystatin or Miconazole oral gel 155  Localized Neonatal Infections Diaper Dermatitis Candida albicans Intensely erythematous confluent plaque with a scalloped border and sharply demarcated edge Satellite pustules on contiguous skin Tx: Antifungal cream 156  Localized Neonatal Infections Omphalitis Due to inadequate care of umbilical cord Necrotic tissue serves as an excellent medium for growth May spread to abdominal wall, peritoneum Tx: Antibiotic ointment or oral antibiotics 157  Localized Neonatal Infections Ophthalmia Neonatorum Caused by passage through vaginal canal or through inoculation by contaminated fingers Neisseria gonorrhea (2 – 5 days), Chlamydia trachomatis (5 – 14 days) May lead to blindness or permanent eye damage Redness and swelling of the conjunctiva, edema of eyelids, discharge 158  Localized Neonatal Infections Ophthalmia Neonatorum Tx: – Gonococcal: Ceftriaxone 50mg/kg for 1 dose or Cefotaxime 100mkday, Saline irrigation – Chlamydia: Oral Erythromycin for 2 weeks 159  Neonatal Pneumonia Etiologic agents depend on timing of infection and mode of transmission Signs and symptoms vary from nonspecific to full blown respiratory distress Signs of pneumonia may be difficult to assess in neonates Radiographs: Infiltrates 160  Neonatal Pneumonia Congenital Pneumonia – Cytomegalovirus, Rubella, Treponema pallidum Early – GBS, Gram (-) enteric bacteria, HSV, Candida Late – health-care associated, or community – acquired 161  Neonatal Pneumonia Treatment – 1st 7 – 10 days: Amipicillin + Aminoglycoside or Cefotaxime – 2nd week of life: Ampicillin or Vancomycin + Aminoglycoside 162  Neonatal Meningitis From pathogens from blood or from open NTDs May be associated with sepsis or as a local meningeal infection Lumbar Puncture (LP) as diagnosis Tx – Meningitic dose of Ampicillin – Vancomycin – staphylococcal infection 163  Neonatal Sepsis Infection – suspected or proven condition caused by any pathogen or clinical syndrome associated with high probability of infection Systemic Inflammatory Response Syndrome (SIRS) – infection and subsequent systemic response 164  Neonatal Sepsis Systemic Inflammatory Response Syndrome (SIRS) – infection and subsequent systemic response – At least 2 of the following criteria, 1 of which must be abnormal temperature or WBC count Core temp >38.5 C or 2 SD above normal for age), Bradycardia (2 SD above normal Increased or decreased WBC Count for age 165  Neonatal Sepsis SIRS 166  Neonatal Sepsis Sepsis – SIRS in response to infection Severe Sepsis – Sepsis plus 1 of the following: Cardiovascular organ dysfunction or acute respiratory distress syndrome (ARDS) or >2 other organ dsfunctions 167  Neonatal Sepsis 3 types 1. Early - onset Sepsis – birth to 7 days 2. Late onset – 7 to 30 days 3. Late Late – onset - >30 ays 168 Neonatal Sepsis 169  1. Early - Onset Sepsis Caused by either intrauterine or intrapartum transmission from mother’s GUT Most common bacteria: GBS, E. coli, Klebsiella, Listeria, H. influenzae Identify high-risk neonates for developing sepsis 170  1. Early - Onset Sepsis Major perinatal risk factors – Prematurity 18 hours – Maternal chorioamnionitis or systemic maternal infection – Maternal GBS colonization – Maternal UTI – Fetal distress during intrapartal monitoring 171  1. Early - Onset Sepsis Laboratory work-up – Blood culture – CBC with WBC differential – CSF Examination – CXR – Acute Phase Reactants (ESR, CRP) – Lumbar Puncture (LP) – should be done if with signs and symptoms of sepsis, documented bacteremia or with no response to antibiotics 172  1. Early - Onset Sepsis Treatment – Penicillin + Aminoglycoside – Once pathogen is isolated, start antibiotics according to sensitivities – Cultures (-) and condition has low probability of infection in 48 – 72 hours: discontinue antibiotics – Usually requires 10 – 14 days of effective antimicrobial treatment – If meningitis suspected -> adjust antibiotics to meningitic dose 173  2. Late – Onset, 3. Late Late - Onset Sepsis Late – onset – acquired after delivery in hospital or community Late late – onset – most usually a health care-associated infection (HCAI) in an infant requiring prolonged intensive care Consider special clinical manifestations, possible mode of transmission and environment 174  2. Late – Onset, 3. Late Late - Onset Sepsis Nonspecific signs and symptoms Hematogenous spread that can lead to focal infections (meningitis, osteomyelitis, UTI, arthritis 175  Treatment Empiric Antibiotic Therapy Preferable to obtain specimen prior to antimicrobial inititation Should not be delayed in clinically ill patients Early – onset : Ampicllin + Aminoglycoside or Cefotaxime Late - Onset: Oxacillin, Nafcillin or Vancomycin + Aminoglycoside If with recent antimicrobial therapy: Ceftazidime, Piperacillin – Tazobactam + Aminoglycoside 176  Treatment Directed Antibiotic Therapy Once pathogen has been identified and susceptibility determined, the most appropriate antimicrobial should be given 177  Congenital Infections Acquired by transplacental transmission to the fetus during 1st trimester to early third trimester TORCH ((Toxoplasmosis, Other Infections, Rubella, Cytomegalovirus (CMV) and Herples Simplex Virus (HSV)) Infection 178  Congenital Infections Other infections – Syphilis – HIV – Varicella – Parvovirus B19 – Hepatitis B 179  Congenital Toxoplasmosis Toxoplasma gondii Cats as definite hosts From ingestion of food that contains cysts or oocytes from infected cats Acute infection during pregnancy -> transplacental transmission Risk of infection correlates directly with gestational age at which maternal infection occurs 180  Congenital Toxoplasmosis Classic triad: Hydrocephalus + Chorioretinitis + Intra-cerebral calcifications SGA, Jaundice, Hepatosplenomegaly, generalized maculopapular rash Increased risk for neurolic and neurodevelopmental complications Diagnosis: Serologic Testing Tx: Pyrimethamine + Sulfadiazine Pregnant mothers should avoid cat exposure and eat well cooked-meat 181  Congenital Syphilis Treponema pallidum Vertical transmission rate of 100% Most are asymptomatic at birth but may develop within weeks or months Early signs during first year of life Late signs during the 1st 2 decades Clinical Manifestaions – Anemia, thrombocytopenia, pneumonitis, osteochondritis or perichondritis, peristent rhinitis “snuffles”, mucocutaneous lesions, desquamative rashes over palms and soles 182 Congenital Syphilis 183 Congenital Syphilis 184  Congenital Rubella Syndrome From Rubella virus Acquired early in gestation First trimester: Congenital defects in 85% of infants, 40% of which may spontaneously abort Defects are rare if >20 weeks AOG 185  Congenital Rubella Syndrome Growth retardation Hepatosplenomegaly Purpuric skin lesions (blueberry muffin spots) 186  Congenital Rubella Syndrome Diagnosis: Isolation of virus (Blood, urine, throat swab, CSF), Rubella specific IgM or IgG Tx: No specific treatment Give supportive care Isolate for 7 days after onset of rash Practice standard plus droplet precaution May excrete in respiratory secretions for up to 1 year 187  Neonatal Herpes Simplex Mostly caused by HSV-2 Transmission is in utero, intrapartum or post-natal Symptoms appear at 5 – 10 days of life 3 patterns of disease – Localized to skin, eyes or mouth (SEM Disease) – Encephalitis – Disseminated infection 188  Neonatal Herpes Simplex 1. Vesicular lesions to the skin, eye and mouth at 5 – 11 DOL 2. Encephalitis at 8 – 17 DOL, findings of meningitis 3. Disseminated HSV have findings similar to sepsis 189  Neonatal Herpes Simplex Diagnosis: Isolation of virus or viral DNA by PCR Treatment: Acyclovir IV 190  Congenital Varicella Syndrome In utero infection during 1st and 2nd trimester Clinical Manifestations – Cicatricial skin scarring n zoster like distribution – Limb hypoplasia – CNS and renal abnormalities Diagnosis: Maternal History + Clinical findings in the neonate No specific treatment; supportive care May not isolate patient because of absence of viral shedding 191 Congenital Varicella Syndrome 192  Neonatal Varicella Born to mothers who contracted varicella from 5 days prior to 2 days after the delivery High viral load and causes severe varicella Treatment – Varicella-Zoster Immune Globulin (VZIG) given at birth or within 96 hours – Parenteral Acyclovir in infants who develop lesions Isolate patients n strict airborne precaution isolation for at least 7 days after onset of rash 193  Neonatal CMV Infection Most common cause of congenital infection Clinical Manifestations – Microcephaly, IUGR, thrombocytopenia, hepatosplenomelagy, jaundice, intracranial periventricular celcifications, chorioretinitis, sensorineural hearing 194 defects  Neonatal CMV Infection Neurologic manifestations later in life Diagnosis: Isolation of virus by PCR Infants chronically excrete CMV in their urine for several years No approved antiviral agents 195  Thank You! References – NTP, 20th Edition: Part XII The Fetus and Neonatal Infant – Fundamentals of Pediatrics: Chapter 17 Diseases and Problems in the Newborn 196