1.1 Diseases and Problems in the Newborn Trans.pdf

LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS HIGH-RISK PREGNANCY Diseases and Problems in the Newborn...

LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS HIGH-RISK PREGNANCY Diseases and Problems in the Newborn  Increase the likelihood of poor outcome during (Part 1) pregnancy, delivery and postneonatal period. Paula Michelle M. Perez, MD  10-20% of pregnant women can be identified as being high-risk NEONATAL PERIOD  Factors associated with High-Risk Pregnancy  Period between birth until 28th day of life 1. Genetic Factors  Further subdivided into: 2. Maternal Factors  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 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 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. 1|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS 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 2. MATERNAL FACTORS  Age for least risk for neonatal mortality: 20 – 30 years old  Maternal illness  Multiple pregnancies  Infections  Certain drugs  In vitro fertilization  Examine the placenta, cord and membrane  Preterm birth – PROM, cervical shortening,  Fetal blood loss – placental pallor, infection retroplacental hematoma, tears in  Polyhydramnios, oligohydramnios velamentous cords  Placental edema – hydrops fetalis, congenital nephrosis or hepatic disease REVIEW  Small whitish nodules on the cord – Polyhydramnios indicates amniotic fluid of >2,000 ml candidal infection during the third trimester, while oligohydramnios has  Single umbilical arteries – congenital renal a volume of 4, 000 grams  Most important factors: Maternal Diabetes and Obesity  Infants of Diabetic Mothers (IDM)  Macrosomia  Excess delivery of nutrients to the fetus CEPHALHEMATOMA  Result in fetal hyperglycemia,  Subperiosteal collection of blood hyperinsulinemia, increased growth  Unilaterally, parietal bone  Greater shoulder and extremity  Firm, tense mass circumference, body fat, upper extremity  DOES NOT CROSS SUTURE LINES skin fold, decreased ratio of head-to-  Complete resolution after 6 weeks abdominal circumference  Most common complication: Skull fracture,  Complications intracranial hemorrhage  Increased likelihood of CS delivery  Predisposes mother to lacerations, postpartum hemorrhage  Birth injuries: brachial plexus injury, clavicular fracture, shoulder dystocia  Polycythemia  Perinatal asphyxia due to increased oxygen utilization and complications of delivery  Monitor glucose levels BIRTH INJURIES  Any adverse effects sustained by an infant during the birthing process  Caused by mechanical factors  Risk factors  Macrosomia  Prematurity  Cephalopelvic disproportion  Dystocia  Prolonged labor  Abnormal presentation  Operative deliveries (vacuum, forceps) 6|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS  90% undergo complete spontaneous deliver  Observe for at least 1 year before surgery  Surgical intervention: Decompression or Neuroplasty NECK, SHOULDER AND CHEST INJURY CLAVICULAR FRACTURE  Most common birth injury  Major causes: Difficult shoulder delivery in vertex presentation; difficult extended arm delivery in breech presentation  Clinical Manifestation  Presence of callus 7 – 10 days after birth  Lack of movement and moro reflex on the SUBGALEAL HEMORRHAGE affected side  Bleeding below the aponeurosis  Radiograph to confirm the diagnosis  Most common cause: Instrumental deliveries  Treatment  Firm, fluctuant mass, increasing in size after  Immobilize, limit the pain birth  Monitor neonate closely for blood loss, BRACHIAL PLEXUS PALSY coagulopathy, and hyperbilirubinemia  3 types of injury  Blood transfusion, address hypovolemic  Erb-Duchenne – upper arm paralysis, C5 – shock C6  May resolve in 2 – 3 weeks  Klumpke – lower arm paralysis C8 - T1  Morbidity is high as 25%  Paralysis of the whole arm  Main predisposing factor: Prolonged labor  Clinical Manifestations  Erb-Duchenne o internal rotation and adduction of the affected arm with elbow extension, forearm pronation and wrist flexion; grasp reflex intact  Klumpke o hand, long flexors of wrist and fingers of affected arm are involved, FACIAL INJURY grasp reflex absent  Paralysis of the whole arm FACIAL NERVE PALSY o limp, motionless and powerless affected arm  Due to pressure over the facial nerve  Initial conservative management with closer  Most common contributing factor: Prolonged 2nd follow-ups stage of labor and forceps delivery  Daily exercises  Clinical manifestation  More apparent on Day 1 – 2 of life  No significant improvement after 3 months ->  Central Paralysis surgical intervention o localized to 1 side, forehead and eyelid movement not affected  Peripheral Paralysis o forehead and eyelid are also involved BrachialPlexusPalsy 7|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS RESPIRATORY DISORDERS HYPEROXIA TEST  Deliver 100% oxygen in terms and 90 – 95% in REVIEW preterms In utero, the placenta serves as the organ for gas  If oxygenation improves and saturation reading exchange for the fetus. is >95%, then the respiratory distress is most likely respiratory in origin The pulmonary vessels of the fetus are vasoconstricted or vasodilated in utero. HYPEROXIA – HYPERVENTILATION TEST  Differentiate cyanotic CHD from Persistent The normal respiratory rate for a neonate is 40-60 Pulmonary Hypertension in the Newborn breaths per minute. (PPHN)  Hyperventilation is applied and if oxygen saturation improves, then the patient has PPHN  Most frequent cause of admission in NICU  Transition from fetal to neonatal respiration APNEA involves several process  Mostly in preterms; varies inversely with  Three major changes gestational age  Cessation of breathing for longer than 20 seconds or for any duration if accompanied by cyanosis and bradycardia  Treatment Bradypy o48  Gentle tactile stimulation  Methylxanthines (Caffeine and Theophylline)  Resolves by 37 weeks postconceptional age SURFACTANTS TRANSIENT TACHYPNEA OF THE NEWBORN (TTN)  Consist of lecithin, phosphatidylcholine,  Risk factors Tachypnea surfactant proteins and cholesterol  CS Delivery  Produced by Type II pneumocytes Claracells  Precipitous birth  Infants of Diabetic Mother (IDM)  Main function: Reduce surface tension  Pathogenesis:  Prevent collapse of small air spaces at end-  Delayed resorption of fetal lung fluid expiration  Clinical Manifestations  Help maintain Functional Residual Capacity  Persistently high respiratory rate (60 – (FRC) 35wks If skffHfe 100 cycles per minute) lungs  About 30 – 40 % oxygen is required RESPIRATORY SIGNS AND SYMPTOMS  Resolves after 48 – 72 hours  Diagnosis  Radiograph: Central perihilar streaking  Treatment  Mainly supportive with supplemental oxygen  Prognosis  Self-limiting  No risk of recurrence  No residual effects nor complications 8|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS RESPIRATORY DISTRESS SYNDROME (RDS)  Treatment  Or Hyaline Membrane Disease  Surfactant administration  Most common etiology of respiratory distress  Supportive care and cause of NICU admission  Recommended range of oxygen saturation  Occurs in preterm babies, with risk of RDS is 91 – 95% inversely proportional to the age of gestation  Prevention (AOG) of the patient  Avoidance of unnecessary induction of labor  Contributing factors  Administer antenatal corticosteroids  Maternal DM (Dexamethasone or Betamethasone) before Trouctionofcurtain  Multiple births 34 weeks AOG  CS Delivery  Asphyxia NEONATAL PNEUMONIA  Maternal history of previously affected  Common Risk Factors infants  Prematurity  Primary Cause: SURFACTANT DEFICIENCY  Premature rupture of membranes (PROM)  Pathophysiology: Failure to attain adequate FRC  Intrapartum maternal fever and tendency of the lungs to become atelectatic  Chorioamnionitis  Mature levels of pulmonary surfactant is present  Most common etiologic agent: Escherichia coli virus at 34 – 36 weeks AOG  Clinical Manifestations: Signs of respiratory  Lecithin/Sphingomyelin (L/S) Ratio of 2:1 distress indicates fetal lung maturity  Diagnosis  Clinical Manifestations  Radiograph: Infiltrates, streaky densities,  Increasing distress and hypoxia on the first lung consolidation 72 hours of life, may appear within minutes  Laboratories: CBC, Blood culture of birth  Treatment  Breath sounds may be normal but crackles  Ampicillin + Amikacin or Gentamicin may be present  Duration of treatment depends on blood CS  If untreated, there is worsening of dyspnea and cyanosis MECONIUM ASPIRATION SYNDROME  In most cases, the signs reach a peak within  Meconium-stained amniotic fluid (MSAF) is 3 days, after which improvement is gradual found in 10 – 15% of births  Diagnosis:  Risk Factors for MSAF o Clinical Course + Chest Xray +  Postmaturity Laboratory Findings  SGA  Chest Xray: Reticulogranular pattern, Ground  Fetal distress Glass Appearance, Air bronchograms  Placental insufficiency  Laboratory findings consistent with hypoxemia,  Cord compression hypercapnia and acidosis  ~5% of live births develop into Meconium Aspiration Syndrome (MAS) 9|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN)  Often idiopathic  Predisposing factors  Birth asphyxia  MAS  Early-onset sepsis  RDS  Hypoglycemia  Pulmonary hypoplasia  Polycythemia  NSAID use  SSRI use  PULMONARY HYPERTENSION leading to severe hypoxemia  Persistent hypoxemia and acidemia caused by pulmonary, cardiac, metabolic or infectious process  Clinical Manifestations  Persistence of right – to – left shunting murmurs  Respiratory distress  Clinical Manifestations  Barrel-chest  Respiratory distress within the 1st 12 hours  Usually improves within 72 hours but if after birth severe, with high risk of mortality  O2 administration does not relieve the  Diagnosis respiratory distress  Chest radiograph: Patchy infiltrates with  Increase requirement of PIP or PEEP streaking of both lung fields, flattening of the  Diagnosis diaphragm and increased anteroposterior  Hyperoxia - Hyperventilation Test diameter  Echocardiography – gold standard  Treatment  Complex and individualized  Preventive measures against occurrence of PPHN should be done  Supportive care  Use of inhaled Nitric Oxide (NO)  Sildenafil vasodilation  Extracorporeal howpulmonary Adultare heymembrane oxygenation (ECMO)  Prognosis  High mortality  20% risk of rehospitalization within 1 year of discharge  High risk of audiologic, neurodevelopmental and cognitive impairments  Complications  Pneumothorax, pneumomediastinum CONGENITAL DIAPHRAGMATIC HERNIA (CDH)  PPHN  Communication between the abdominal and  Neurologic sequelae thoracic cavity  Prognosis  Forms: Bochdalek (posterolateral), Morgagni o depends on the neurologic status if (retrosternal), hiatal, paraesophageal hypoxia is not immediately corrected  Major limiting factor for survival is PULMONARY HYPOPLASIA 10 | P a g e  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS  Diagnosis  Clinical Manifestations  Prenatal Ultrasonography  Cephalocaudal progression  CXR after delivery  Indirect bilirubin – bright yellow or orange  Clinical manifestations  Direct – greenish or muddy yellow cast  Cardinal sign: Respiratory distress  Kernicterus – lethargy, poor feeding metanoiaencephalopathy  Scaphoid abdomen and increased chest wall diameter  Bowel sounds at the chest wall  Point of cardiac impulse displaced  Treatment  Rapid intubation; Avoid prolonged mask ventilation  Maintain oxygenation and carbon dioxide elimination without inducing volutrauma  Surgical repair  Overall survival is 67% with spontaneous demise at 7 – 10% DIGESTIVE SYSTEM DISORDERS NEONATAL HYPERBILIRUBINEMIA REVIEW  Etiology of unconjugated hyperbilirubinemia Physiologic jaundice usually lasts for 7 days for term neonates and 14 days for preterm babies. If jaundice occurs as early as 24 hours of life of the baby, then it is considered pathologic. NEONATAL HYPERBILIRUBINEMIA  60% of term, 80% of preterm  Onset and duration depends on etiology   3 main mechanisms  Shorter lifespan of erythrocytes at 70 – 90 KERNICTERUS days NormalRBClifespan 120 days  Bilirubin encephalopathy  Low number of bacteria in neonatal intestine  Deposition of unconjugated bilirubin in the basal and decreased activity of beta- ganglia and brainstem nuclei glucoronidase  >20mg/dL  Decreased activity of ligandin  The more immature the infant is, the greater the susceptibility to kernicterus 11 | P a g e  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS  Clinical Manifestations  Distal part of ileum and proximal segment of  Term – 2 – 5 days; Preterms – 7 days colon  Subtle early signs  Triad  Initial signs: lethargy, poor feeding, loss of  Injury – intestinal ischemia Moro reflex  Metabolic substrate – enteral nutrition  Opisthotonos with bulging fontanel  Bacterial translocation  Shrill, high-pitched cry  Prematurity as greatest risk factor  Convulsions and spasm  Characteristic histologic finding: Coagulation  Prevention necrosis  Practical, system-based approach  Recommendations Clinical Manifestation  Evaluate jaundice 35 weeks AOG for treatment of hyperbilirubinemia Treatment  Complications  Prevent further injury; NPO, nasogastric  Loose stools, erythematous macular rash, decompression dehydration, hypothermia  Systemic broad spectrum antibiotics  Bronze Baby Syndrome – dark – grayish  Parenteral fluids brown skin discoloration  Supportive care  Exchange transfusion – double volume  Indications for surgery exchange transfusion (DVET), partially remove o Perforation on abdominal xray hemolyzed and anti-body coated RBCs and o Positive result of abdominal replace with donor RBCs paracentesis  Indications for exchange transfusion o Failure of medical management  Failure of phototherapy  Mortality in 30 – 40% of severe cases  Continued hemolysis  Kernicterus  For direct hyperbilirubinemia, Phototherapy and exchange transfusion is not indicated  Ursodeoxycholic acid (UDCA) is the drug of choice  Surgical procedure  Treat infection 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 12 | P a g e  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS o Jaundice on 1st 24 hours, may reach Diseases and Problems in the Newborn high levels causing bilirubin (Part 2) encephalopathy Paula Michelle M. Perez, MD  Diagnosis o (+) Direct Coombs Test HEMATOLOGIC DISORDERS o Anemia o Polychromasia in PBS ANEMIA IN THE NEWBORN INFANT o Hyperbilirubinemia  Physiologic anemia o Antenatal Diagnosis: Percutaneous o Term: 8 – 12 weeks (Hgb 11 g/dL) Umbilical Blood Sampling o Preterm: 6 weeks (7 – 10 g/dL)  Treatment o DVET  Anemia of prematurity o Intravenous Immunoglobulin o LBW 1- 3 months after birth o Hgb 2 weeks, due to Vitamin K HEMOLYTIC DISEASE OF THE NEWBORN malabsorption  Erythroblastosis fetalis  Breastmilk – poor source of Vitamin K  Transplacental passage of maternal antibody  Prevention: Vitamin K 1 mg IM at birth active against paternal RBC antigens  Treatment  Increased rate of RBC destruction o Vitamin K 1 – 5 mg IV infusion o Blood transfusion of Fresh Frozen ABO Incompatibility Plasma or whole blood  Most common cause of hemolytic disease in the newborn NERVOUS SYSTEM DISORDERS  Mother – type O, Baby – type A or B  Clinical Manifestations NEONATAL SEIZURES o Jaundice in the 1st 24 hours  Classified according to the most prominent  Diagnosis component o ABO incompatibility o Subtle o (+) Direct Coomb’s test o Focal clonic o Spherocytes in PBS o Multifocal clonic o hyperbilirubinemia o Focal or generalized tonic  Treatment o Myoclonic o Phototherapy o Spasm o Severe cases: IVIg administration, o Tonic - clonic DVET  Neonatal Seizures  May be post-asphyxial, hemorrhagic, metabolic, Rh Incompatibility toxic, infectious and genetic  Clinical Manifestations  Benign jitteriness o May range from mild hemolysis to  Rapid, tremuluos movement of short – duration severe anemia  Triggered by sensory stimulus o Hydrops fetalis – excessive abnormal  Abates with restraint or repositioning of the fluid in 2 or more fetal compartments infant  Diagnosis: Careful prental, perinatal and family history, complete PE and neurologic exam 1|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS HYPOXIC – ISCHEMIC ENCEPHALOPATHY (HIE)  Clinical Manifestations  Caused by hypoxia and ischemia to the CNS, o Majority have no initial clinical signs which frequently occurs perinatally o Acute deterioration in 2nd – 3rd DOL  Important cause of permanent CNS damage o Pallor, cyanosis, poor suck, seizures,  Maybe due to different factors shock, decreased muscle tone o Inadequate oxygenation o PVL is clinically asymptomatic and o Low maternal blood pressure becomes apparent in later infancy as o Placental insufficiency spastic deficits o Abruptio placenta  Diagnosis o Cord prolapse o History + Clinical Manifestations  Clinical Manifestations o Cranial UTZ – preferred imaging o Severity would depend on the duration technique and timing of injury o All at-risk infants should undergo follow- o At birth, depressed neonates with no up ultrasonography spontaneous respiration o Pallor, cyanosis, apnea o Cerebral edema may develop during the next 24 hours o Systemic organ dysfunction in up to 80% of affected neonates  Diagnosis o Diffusion – weighted MRI – preferred imaging modality o Cranial Ultrasonography – in preterm  Treatment o Establish and maintain adequate ventilation and perfusion o Treat and control seizures o Amplitute integrated EEG (aEEG) to  ~3 – 5% of VLBW develop Posthemorrhagic prognosticate brain injury Hydrocephalus (PHH), sometimes requiring o Systemic or selective cerebral ventriculoperitoneal (VP) shunt hypothermia  Degree of IVH and PVL strongly linked to neurodevelopmental impairment INTRACRANIAL HEMORRHAGE  Treatment  May be caused by trauma or asphyxia; rarely by o Treat and control seizures primary hemorrhagic disturbance or congenital o Correct anemia and coagulopathy vascular anomaly o Supportive care  Intraventricular hemorrhage (IVH) on preterm  Prevention infants o Improved perinatal care and decrease o Risk is inversely related to gestational risk for preterm delivery age and birth weight o Antenatal corticosteroids at 24 – 34 o Predisposing factors: Prematurity, RDS, weeks for mothers at risk for preterm Hypoxic – ischemic or hypotensive delivery injury, reperfusion injury of damaged vessels, abnormal cerebral blood flow  Periventricular Leukomalacia (PVL) o Neonates < 1,000 grams o Focal necrotic lesion un the periventricular white matter o Increased occurrence with neonates with severe IVH 2|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS REVIEW  Treatment Maternal folic acid supplementation at dose of 0.4 o Multidisciplinary approach mg once a day is recommended to reduce the o Evaluate and address other congenital incidence of Neural Tube Defects (NTD). anomalies o Surgical procedure If NTD was noted on previous pregnancy, the dose of  Prognosis Folic Acid should be given at 4 g once a day ideally o Renal dysfunction as most important 1 month preconception. determinants of mortality ANENCEPHALY NEURAL TUBE DEFECTS  Large defect of the calvarium, meninges and  Failure of the neural tube to close spontaneously scalp between 3rd – 4th week AOG  Rudimentary brain  Absent cerebrum and cerebellum SPINA BIFIDA OCCULTA  Infants die within several days after birth  Occult spinal dysraphism  Midline spinal defect without protrusion of spinal MICROCEPHALY cord or meninges  Head circumference 3 SD below the mean for  Asymptomatic patients age and sex  Cutaneous manifestations: hemangioma,  Main groups: Primary and Secondary discoloration of the skin, pit, lump, dermal sinus,  Diagnosis hairy patch o Serial head circumference  Diagnosis measurement o UTZ – initial screening o MRI – identify structural abnormalities o MRI – more accurate o TORCH assay  Treatment MENINGOCOELE o Provide accurate family counseling  Meninges herniate through a defect in posterior o Refer to subspecialist vertebral arches or anterior sacrum  Spinal cord usually normal HYDROCEPHALUS  Fluctuant midline mass that might  Abnormal accumulation of cerebrospinal fluid transilluminate (CSF) within the ventricular system  Thorough diagnostics before surgical procedure  Communicating or noncommunicating  Clinical Manifestations MYELOMENINGOCOELE o Depends on many factors  Represents most severe form of dysraphism o Age  Herniation of spinal cord and meninges through o Nature of lesion a defect un the bony spinal canal o Duration and increase of intracranial  Clinical Manifestations pressure o Dysfunction of many organs and  Treatment structures o Identify cause o Most common: Lumbosacral region o Determine extent and associated o Low sacral region: bowel and bladder lesions incontinence o VP Shunting o Increased neurologic deficit as the o Planning for long-term follow-ups defect extends higher into the thoracic region o Consider possibility of hydrocephalus no matter the spinal level 3|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS NEONATAL INFECTIONS LOCALIZED NEONATAL INFECTIONS  Important cause of neonatal morbidity and mortality ORAL THRUSH  Unique due to:  Oral Pseudomembranous candidiasis o Diverse modes of transmission  Candida albicans o Immunologic immaturity  White patches inside the cheeks and tongue o Coexisting conditions  Tx: o Varying clinical manifestations o Oral Nystatin or Miconazole oral gel o Wide variety of agents  Modes of Transmission DIAPER DERMATITIS o Intrauterine  Candida albicans  Either transplacental route  Intensely erythematous confluent plaque with a (horizontal transmission) or scalloped border and sharply demarcated edge transcervical (ascending  Satellite pustules on contiguous skin transmission)  Tx: o Intrapartum o Antifungal cream o Post-natal OMPHALITIS INTRAUTERINE INFECTION - TRANSPLACENTAL  Due to inadequate care of umbilical cord INFECTION  Necrotic tissue serves as an excellent medium  Result of clinical or subclinical maternal infection for growth  Timing of infection affects the outcome  May spread to abdominal wall, peritoneum  Tx: INTRAUTERINE INFECTION - TRANSCERVICAL o Antibiotic ointment or oral antibiotics INFECTION  Membranes rupture and infant passes through OPHTHALMIA NEONATORUM the birth canal  Caused by passage through vaginal canal or  Chroioamnionitis through inoculation by contaminated fingers o Microbial invasion of amniotic fluid from  Neisseria gonorrhea (2 – 5 days), Chlamydia prolonged rupture of membranes trachomatis (5 – 14 days) o Maternal fever ± signs of  May lead to blindness or permanent eye chorioamnionitis damage o Directly related to duration of rupture of  Redness and swelling of the conjunctiva, edema membranes of eyelids, discharge o 18 hours - cutoff  Tx: o Gonococcal: Ceftriaxone 50mg/kg for 1 POST - NATAL dose or Cefotaxime 100mkday, Saline  From exposure in the nursery or to the irrigation community (including family) o Chlamydia: Oral Erythromycin for 2  Hospitalized newborns: Hand contamination weeks NEONATAL PNEUMONIA EARLY VS LATE ONSET  Etiologic agents depend on timing of infection EARLY – ONSET LATE – ONSET and mode of transmission  Signs and symptoms vary from nonspecific to acquired before or during after delivery; from hospital full blown respiratory distress delivery or community  Signs of pneumonia may be difficult to assess in Age at onset depends on timing of exposure and neonates virulence of infecting organism  Radiographs: Infiltrates 4|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS  Congenital Pneumonia – Cytomegalovirus, Rubella, Treponema pallidum  Early – GBS, Gram (-) enteric bacteria, HSV, Candida  Late – health-care associated, or community – acquired  Treatment o 1st 7 – 10 days: Amipicillin + Aminoglycoside or Cefotaxime o 2nd week of life: Ampicillin or Vancomycin + Aminoglycoside 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 o Meningitic dose of Ampicillin 1. EARLY - ONSET SEPSIS o Vancomycin – staphylococcal infection  Caused by either intrauterine or intrapartum transmission from mother’s GUT NEONATAL SEPSIS  Most common bacteria: GBS, E. coli,  Infection – suspected or proven condition Klebsiella, Listeria, H. influenzae caused by any pathogen or clinical syndrome  Identify high-risk neonates for developing sepsis associated with high probability of infection  Major perinatal risk factors  Systemic Inflammatory Response Syndrome o Prematurity 18 hours response o Maternal chorioamnionitis or systemic maternal infection At least 2 of the following criteria, 1 of which must be o Maternal GBS colonization abnormal temperature or WBC count o Maternal UTI o Fetal distress during intrapartal 1. Core temp >38.5 C or 2 SD above normal for age),  Laboratory work-up Bradycardia (2 SD above normal o CBC with WBC differential 4. Increased or decreased WBC Count for age o CSF Examination o CXR  Sepsis – SIRS in response to infection o Acute Phase Reactants (ESR, CRP)  Severe Sepsis – Sepsis plus 1 of the following: o Lumbar Puncture (LP) – should be done Cardiovascular organ dysfunction or acute if with signs and symptoms of sepsis, respiratory distress syndrome (ARDS) or >2 documented bacteremia or with no other organ dysfunctions response to antibiotics  Treatment  3 types o Penicillin + Aminoglycoside o Early - onset Sepsis – birth to 7 days o Once pathogen is isolated, start o Late onset – 7 to 30 days antibiotics according to sensitivities o Late Late – onset - >30 ays o Cultures (-) and condition has low probability of infection in 48 – 72 hours: discontinue antibiotics 5|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS o Usually requires 10 – 14 days of CONGENITAL TOXOPLASMOSIS effective antimicrobial treatment  Toxoplasma gondii o If meningitis suspected -> adjust  Cats as definite hosts antibiotics to meningitic dose  From ingestion of food that contains cysts or oocytes from infected cats 2. LATE – ONSET, 3. LATE LATE - ONSET SEPSIS  Acute infection during pregnancy ->  Late – onset – acquired after delivery in hospital transplacental transmission or community  Risk of infection correlates directly with  Late late – onset – most usually a health care- gestational age at which maternal infection associated infection (HCAI) in an infant requiring occurs prolonged intensive care  Classic triad:  Consider special clinical manifestations, o Hydrocephalus possible mode of transmission and environment o Chorioretinitis  Nonspecific signs and symptoms o Intra-cerebral calcifications  Hematogenous spread that can lead to focal  SGA, Jaundice, Hepatosplenomegaly, infections (meningitis, osteomyelitis, UTI, generalized maculopapular rash arthritis  Increased risk for neurolic and  Treatment neurodevelopmental complications  Diagnosis: Empiric Antibiotic Therapy o Serologic Testing  Preferable to obtain specimen prior to  Tx: antimicrobial inititation o Pyrimethamine + Sulfadiazine  Should not be delayed in clinically ill patients  Pregnant mothers should avoid cat exposure  Early – onset : Ampicllin + Aminoglycoside or and eat well cooked-meat Cefotaxime  Late - Onset: Oxacillin, Nafcillin or Vancomycin CONGENITAL SYPHILIS + Aminoglycoside  Treponema pallidum  If with recent antimicrobial therapy: Ceftazidime,  Vertical transmission rate of 100% Piperacillin – Tazobactam + Aminoglycoside  Most are asymptomatic at birth but may develop within weeks or months Directed Antibiotic Therapy  Early signs during first year of life Once pathogen has been identified and susceptibility  Late signs during the 1st 2 decades determined, the most appropriate antimicrobial should  Clinical Manifestaions be given o Anemia, thrombocytopenia, pneumonitis, osteochondritis or perichondritis, CONGENITAL INFECTIONS peristent rhinitis “snuffles”,  Acquired by transplacental transmission to the mucocutaneous lesions, desquamative fetus during 1st trimester to early third trimester rashes over palms and soles  TORCH o Toxoplasmosis o Other Infections o Rubella o Cytomegalovirus (CMV) o Herples Simplex Virus (HSV)) Infection  Other infections o Syphilis o HIV o Varicella o Parvovirus B19 o Hepatitis B 6|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS  Diagnosis: o Isolation of virus (Blood, urine, throat swab, CSF), Rubella specific IgM or IgG  Tx: o No specific treatment o Give supportive care o Isolate for 7 days after onset of rash o Practice standard plus droplet precaution o May excrete in respiratory secretions for up to 1 year 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 CONGENITAL RUBELLA SYNDROME o Localized to skin, eyes or mouth (SEM  From Rubella virus Disease) o Encephalitis  Acquired early in gestation o Disseminated infection  First trimester: Congenital defects in 85% of infants, 40% of which may spontaneously abort  Defects are rare if >20 weeks AOG  Growth retardation  Hepatosplenomegaly  Purpuric skin lesions (blueberry muffin spots) 7|Page  LYCEUM-NORTHWESTERN UNIVERSITY – FQDMF MED2022 – SECTION A PEDIATRICS 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  Diagnosis: o Isolation of virus or viral DNA by PCR  Treatment: o Acyclovir IV CONGENITAL VARICELLA SYNDROME  In utero infection during 1st and 2nd trimester  Clinical Manifestations o Cicatricial skin scarring n zoster like distribution o Limb hypoplasia o CNS and renal abnormalities  Diagnosis: o Maternal History + Clinical findings in the neonate  No specific treatment; supportive care  May not isolate patient because of absence of viral shedding  Born to mothers who contracted varicella from 5 days prior to 2 days after the delivery  High viral load and causes severe varicella  Treatment o Varicella-Zoster Immune Globulin (VZIG) given at birth or within 96 hours o Parenteral Acyclovir in infants who develop lesions  Isolate patients n strict airborne precaution isolation for at least 7 days after onset of rash NEONATAL CMV INFECTION  Most common cause of congenital infection  Clinical Manifestations o Microcephaly, IUGR, thrombocytopenia, hepatosplenomelagy, jaundice, intracranial periventricular celcifications, chorioretinitis, sensorineural hearing defects o Neurologic manifestations later in life  Diagnosis: o Isolation of virus by PCR  Infants chronically excrete CMV in their urine for several years  No approved antiviral agents 8|Page