Neonatal Flashcards
fetus and newborn
-Late fetal-early neonatal period has highest mortality rate of any age interval
-Perinatal mortality: Deaths occurring from 20 week of gestation until 28th day after birth
-Neonatal mortality: Deaths occurring from birth to 28th day of life
-Infant mortality rate: Deaths occurring during neonatal and post-neonatal periods
-Low birthweight (LBW): Infants having birthweights of < 2,500 grams -> 40x greater risk of mortality
-Very low birthweight (VLBW): Infants weighing < 1,500 gram -> 200x greater risk of mortality
maternal risk factors
-Previous LBW birth
-Low socioeconomic status
-Low level of education
-Poor antenatal care
-Maternal age < 16 or > 35 years
-Short interval periods between pregnancies
-Cigarette smoking, alcohol, and illicit drug use
-Physical or psychologic stresses
-Single parent
-Low pre-pregnancy weight (< 45 kg)
-Poor weight gain during pregnancy (< 10 lbs)
-Black race (2 x risk)
fetal to neonatal physiology transition
-clamping of umbilical cord:
-Eliminates low pressure system of the placenta and increases systemic BP
-Decreased venous return from placenta decreases right atrial pressure
-breathing begins:
-Air replaces lung fluid
-Pulmonary resistance decreases, increases blood flow to lungs, increases pulmonary venous return to LA – LA pressure > RA pressure = !closure of foramen ovale! :)
-Arterial oxygen tension increases = !ductus arteriosus begins to constrict!
routine delivery room care: Apgar score
-Performed at 1 and 5 mins after birth
-Normal: 8-9 at 1 and 5 minutes
-Close attention: 4-7
-Cardiopulmonary arrest, bradycardia, hypoventilation, or CNS depression: 0-3
-Most with low Apgar scores improve with assisted ventilation via face mask or by ET intubation
routine delivery room care
-Erythromycin (topical) for neonatal gonococcal and chlamydial conjunctivitis prophylaxis
-Antiseptic skin/cord care to prevent spread of pathologic bacteria from one infant to another and to prevent disease in individual infant
-Antibiotic ointment, topical alcohol, or chlorhexidine (defense against gram-positive organisms, like S. aureus)
-Vitamin K prophylaxis (IM) to prevent hemorrhagic disease of the newborn
-Hepatitis B vaccine prior to discharge
-Warmth
-Ideal temperature is neutral thermal environment
-Heat production is via non-shivering thermogenesis due to -> Brown fat: Highly vascular, many mitochondria, surrounds large blood vessels
delivery room resuscitation
-Cyanosis
-Acrocyanosis (hands and feet) is common and usually normal- every a few days after
-Central cyanosis (trunk, mucosal membranes, and tongue) -> any time after birth and is always from serious underlying condition (below)
-Life-Threatening Congenital Malformations
-Choanal atresia and other lesions obstructing the airway
-Intrathoracic lesions: Cysts, diaphragmatic hernias
-Malformations that obstruct the GI tract at level of esophagus, duodenum, or colon
-Gastroschisis (intestinal necrosis), omphalocele
delivery room resuscitation: asphyxia
-Asphyxia w/ severe bradycardia or cardiac insufficiency reduces or stops tissue blood flow -> ischemia
-With severe or prolonged intrauterine/neonatal asphyxia, vital organs affected
-Maternal risk factors: Ds that interfere with uteroplacental perfusion, epidural anesthesia, vena caval compression syndrome, medications
-Fetal/newborn risk factors:
-Immature infants (< 1000 g) – Surfactant deficiency
-Newborns (premature): Respond paradoxically to hypoxia with apnea NOT tachypnea!
-#1 cause of MI in neonates is respiratory related not cardiac
-Episodes of intrauterine asphyxia may depress neonatal CNS –> may not initiate ventilatory response at birth and may undergo another episode of asphyxia
delivery room resuscitation: shock
-Pallor, poor cap refill time, lack of palpable pulses, hypotonia, cyanosis, and eventually cardiopulmonary arrest
-MCC is blood loss before or during labor (hypovolemia)
-Severe intrauterine bacterial sepsis (distributive)– mottled, hypotonic, and cyanotic with diminished peripheral pulses
-Peripheral, symmetric gangrene (purpuric rash) - often sign of hypotensive shock with severe congenital bacterial infections
-Tx:
-Airway stabilization and ventilatory support
-Hypovolemic shock: Repeat boluses of 10-15 cc/kg of normal saline or LR (little bit less than normal hypovolemic shock- dont need to know)
-Anemia: Blood transfusion
-Dopamine, epinephrine, cortisol, as needed
birth injuries (test)
-Caput Succedaneum:
-Diffuse, edematous, dark swelling of soft tissue of scalp that extends across midline and suture lines
-Often following prolonged labor
-boggy
-over the periosteum -> free flowing
-Cephalohematoma:
-Subperiosteal hemorrhage that doesnt cross suture lines surrounding respective bones
-May organize, calcify, and form a central depression
-tx-
-observe- they will absorb
birth injuries: facial nerve injury
-Asymmetric, crying face
-Eye does not close, nasolabial fold absent, side of mouth droops at rest
birth injuries: brachial plexus injury (test)
-Phrenic nerve palsy: C3-5 – May lead to diaphragmatic paralysis/respiratory distress
-Erb-Duchenne paralysis: C5-6 injury – Cannot abduct arm at shoulder, externally rotate arm, or supinate forearm
-Klumpke paralysis: C7-C8, T1 – Paralyzed hand with ipsilateral Horner syndrome, claw hand
-Tx: Supportive, active/passive ROM exercises, nerve grafting
birth injuries: spine/spinal cord injuries
-If excessive force during vertex/breech delivery
-Rotational – C3-4
-Longitudinal – C7-T1
-Spinal cord: Flaccid, apneic, and asphyxiated on PE
birth injuries: clavicle fractures
-usually macrosomic infants (big) after shoulder dystocia
-Asymmetric Moro reflex- briskly drop pt -> if clavicle fractured -> the arm wont go up on that side
-MC birth trauma fracture
-Tx: Immobilization
birth injuries: visceral trauma
-Macrosomic, extremely premature infants
-Liver rupture: Anemia, hypovolemia, shock, hemoperitoneum, and DIC
-Adrenal rupture: Flank mass, jaundice, hematuria
physical exam of newborn: appearance
-Cyanosis, nasal flaring, intercostal retractions, grunting – pulmonary disease
-Meconium staining of umbilical cord/nails/skin –> possible aspiration PNA
-Spontaneous activity, passive muscle tone, quality of cry, apnea – evaluating nervous system
PE of newborn: vital signs
-HR (120-160 bpm)
-RR (30-60 br/min)
-Temperature (rectal)
-BP (reserved for sick infants)
-Length, weight, head circumference- from time of birth
PE of newborn: gestational age (ballard score)
-Determined by assessment of physical signs! and neuromuscular! characteristics
-Signs determined during 1st day of life
-Cumulative score is correlated with a gestational age (accurate to within 2 weeks)
-up until birth we have been estimating age…
-Large for gestational age (LGA): Infants born at a weight > 90th percentile for age (diabetic mother)
-Small for gestational age (SGA): Infants born at a weight < 10th percentile for age
-Values may be utilized to determine age-specific mortality rates!!
-dont need to know chart
PE of newborn: skin
-Eval for pallor, plethora, jaundice, cyanosis, meconium staining, petechiae, ecchymosis, congenital nevi, and neonatal rashes
-Mottling (top photo) and/or acrocyanosis can be in healthy term infant
-mottling from temperature changes
-Lanugo hair and vernix caseosa (soft, white, creamy layer) both disappear by term gestation
-Hair tufts over lumbosacral region –> possible spinal cord defect (spina bifida)
nevi
-Nevus simplex: Salmon patch, pink macular hemangioma
-Nevus flammeus (port-wine stain): May consider Sturge-Weber syndrome -> CNS/convulsions
hemangiomas
-Capillary (raised, red lesions) and cavernous (deeper, blue masses)
-Increase in size after birth, then resolve over 1-4 years
-if extensive or growing -> beta blocker topical
erythema toxicum
Erythematous, papulovesicular rash with eosinophils in vesicular fluid
-normal, self limited
pustular melanosis
-Small, dry vesicles on a pigmented brown macular base
-purulent
-normal, self limited
milia
Yellow-white epidermal cysts of pilosebaceous follicles, typically on nose
miliaria
Prickly heat, obstructed sweat glands
-heat rash
-goes away in 30mins
PE of newborn: skull
-Elongated/molded skull resolves 2-3 days after birth
-Anterior and posterior fontanelles should be soft and non-bulging
-R/o premature closure (synostosis)- restrict brain growth
-Large may signal hydrocephalus, hypothyroidism, rickets
-depressed- dehydration
-Examine for signs of trauma/lacerations from internal fetal electrode site/fetal scalp pH sampling, birth trauma
-Examine for caput succedaneum or cephalohematoma
physical exam of newborn: face
-Inspect for dysmorphic features, asymmetry, tilt
-Epicanthal folds, hypertelorism, preauricular tags/sinuses, low-set ears, long philtrum, cleft lip/palate
-Seventh nerve palsy
-Torticollis
PE of newborn: eyes
-Open spontaneously in upright position
-Assess pupillary response to light and red reflex
-White reflex (leukocoria): Cataracts, ocular tumor, severe chorioretinitis, persistent hyperplastic primary vitreous, or retinopathy of prematurity
-Cloudy cornea: Congenital glaucoma, uveal tract dysgenesis, and storage diseases
-Conjunctival/retinal hemorrhages usually common
PE of newborn: ears
TMs are dull, gray, opaque, and immobile in first 1-4 weeks
PE of newborn: mouth
-Inspect for presence of natal teeth (calcifications), cleft palate, and micrognathia
-Inclusion cysts are normal (Epstein pearls) on hard palate
-Hard, marble-sized masses in buccal mucosa usually transient idiopathic fat necrosis
-all normal
PE of newborn: neck
-Short and symmetric
-Midline clefts (thyroglossal duct cysts), lateral masses (branchial clefts), cystic hygromas, hemangiomas
-Neonatal torticollis!!: Shortening of SCM muscle with fibrous tumor over muscle produces head tilt/abnormal facies -> goes away with PT usually
-vision loss in eye thats not working as much
-Edema/webbing of neck suggest Turner syndrome
-Palpate clavicles for fractures
PE of newborn: chest
-Chest: Inspect wall to identify asymmetry from absence of pectoralis muscle, breast tissue for gestational age/rule out abscess
-!!Supernumerary nipples may signal renal anomalies
-Lungs: Observations of rate, depth, and nature of intercostal/sternal retractions
Breath sounds should be equal, rales resolved by 1-2 hours of life
Diminished/absent: PTX (subcutaneous emphysema), collapsed lung, pleural effusion, or diaphragmatic hernia (bowel sounds in chest)
-Heart
-Position in infants is more midline than in older children
First heart sound is normal, second may not be split in first day of life
-Heart murmurs common, typically transient: Closure of the ductus arteriosus, peripheral pulmonary artery stenosis, or small VSD
-Palpate brachial and femoral pulses
-BP in all pts with a murmur or HF
PE of newborn: abdomen
-Normal liver may be palpable 2 cm below R costal margin, spleen less likely palpable, kidneys palpable in first day of life
-Meconium stool normally passed within 48 hours of birth
-Anus should be patent
-Masses should be evaluated immediately by US
-Abdominal distention may be from obstruction
-Ileal atresia, meconium ileus, midgut volvulus, imperforate anus, or Hirschsprung disease
-check for diaphragmatic hernias
newborn hernias
-Herniation of bowel through abdominal wall 2-3 cm lateral to the umbilicus is a !gastroschisis!
-there is no sac to protect this -> risk of infection and dehydration
-more risk
-Umbilical cord should be inspected –> confirm 2 arteries, 1 vein, and absence of herniation of abdominal contents –> !omphalocele!:
-Bleeding from cord suggests coagulation disorder, chronic discharge may be a granuloma
-Erythema around umbilicus –> !omphalitis! – may cause portal vein thrombophlebitis and subsequent extrahepatic portal HTN)
-know the picture and difference
umbilical cord healing
-bleeding is common
-infection risk though
PE of newborn: genitalia
-Testes should be descended at term -> Occasionally in inguinal canal (cryptorchidism -> testicular ca risk)
-Scrotal swelling: Hernia, transient hydrocele, in utero torsion of testes
-Urethra inspection to r/o epispadias/hypospadias
-Female genitalia: May have milky white/blood-streaked vaginal discharge (from maternal hormone withdrawal)
-Imperforate hymen may cause discharge buildup -> lower midline abdominal mass from enlarged uterus
-Clitoral enlargement with fusion of labia majora -> suggests adrenogenital syndrome or exposure to masculinizing maternal hormones
PE of newborn: neuro/MSK
-Extremities: Eval length, symmetry, and presence of abnormalities
-Spine: Examine for sacral hair tufts, dermal sinus tract above gluteal folds, congenital scoliosis, and soft tissue masses
-Hips: Examine for congenital dysplasia
-Gluteal fold asymmetry or leg length discrepancy (Barlow test and Ortolani maneuver – femoral head displacement, replacement, respectively)
-Neurologic: Evaluate active/passive tone, level of alertness, primary (neonatal) reflexes, deep tendon reflexes (hypereflexive is normal), spontaneous motor activity, and cranial nerves
-palmar reflex- fist around finger
-rooting reflex- finger around mouth- sucking
respiratory distress syndrome (hyaline membrane disease)
-Occurs after onset of breathing and is assoc with insufficiency of pulmonary surfactant
-Surfactant prevents atelectasis by reducing surface tension at low lung volumes when it is concentrated at end expiration as alveolar radius decreases
-Surfactant contributes to lung recoil
-Without surfactant -> surface tensions are not reduced -> atelectasis during end expiration
-ALWAYS THINK THIS FIRST WHEN THERE IS RESPIRATORY DISTRESS
-Risk Factors: Prematurity, low gestational age, delivery of prior preterm infant with RDS, maternal diabetes, hypothermia, fetal distress, asphyxia, males, second-born of twins, and delivery by C-section
respiratory distress syndrome (Hyaline Membrane disease): clinical manifestation
-Initially: Cyanosis, tachypnea, nasal flaring, intercostal/sternal retractions, and GRUNTING (BAD); over 72 hours - increased distress, hypoxemia
-CXR findings: Ground-glass haze surrounding air-filled bronchi or white-out (severe)
-Uncomplicated cases show spontaneous improvement – diuresis and marked improvement of edema
-Severe cases (edema, apnea, respiratory failure) – assisted ventilation
respiratory distress syndrome (Hyaline Membrane disease): complications: PDA
-Patent Ductus Arteriosus
-bc poor oxygenation -> oxygen normally stimulates the closure of PDA
-Less responsive to vasoconstrictive stimuli, complicated by hypoxemia during RDS -> resulting shunt between pulmonary and systemic circulation -> right sided HF, pulmonary edema
-L->R -> increase PVR -> reverses to R ->L -> when you treat you start to overload the pt -> HF
-Widened pulse pressure, peripheral pulses palpable/bounding
-Continuous murmur (systole/diastole)
-HF and pulmonary edema resulting in rales and hepatomegaly
-CXR with cardiomegaly and pulmonary edema; echocardiogram with ductal patency, Doppler with left-to-right flow (back to PA/lungs)
-Treatment
-With RDS: Fluid restriction, diuretic administration; after 1-2 days no improvement –> prostaglandin synthetase inhibitor, ibuprofen, !indomethacin!, or acetaminophen
-Surgical ligation/catheter-based occlusion may be required
respiratory distress syndrome (Hyaline Membrane disease): complications: pulmonary air leaks
-Assisted ventilation may cause overdistention of alveoli > rupture > interstitial emphysema > PTX/pneumomediastinum
-Confirmed by CXR
-Treatment: Symptomatic PTX > pleural chest tube
respiratory distress syndrome (Hyaline Membrane disease): complications: bronchopulmonary dysplasia (chronic lung ds)
-Typically develops following ventilation for RDS complicated by PDA and/or pulmonary air leaks
-Failure of RDS to improve > 2 weeks, need for prolonged ventilation, and oxygen therapy required at 36 weeks of post-conceptual age (development of superoxides, hydrogen peroxide, and free radicals > disrupt membrane) are characteristic
-Clinical Manifestations
-Oxygen dependence, hypercapnia with compensatory metabolic alkalosis, pulmonary HTN, poor growth, development of R-sided HF
-CXR: Lung opacification > cyst development = Sponge-like appearance
-Treatment
-May need mechanical ventilation for several months
-Tracheotomy may be indicated (prevent subglottic stenosis)
-Dexamethasone may reduce inflammation, improve pulmonary function, enhance weaning of pts from ventilation
respiratory distress syndrome (Hyaline Membrane disease): complications: retinopathy of prematurity (retrolental fibroplasia)
-Leading cause of blindness in VLBW infants (< 1500 grams)
-Caused by acute and chronic effects of oxygen toxicity on developing blood vessels of the premature infant’s retina
-Excessive arterial oxygen tensions > vasoconstriction immature retinal vasculature > vaso-obliteration if prolonged
-Subsequent proliferative phase – Extraretinal fibrovascular proliferation > fibrous proliferation behind lens produces leukocoria/displacement of lens > causes glaucoma
-Treatment: Spontaneous resolution versus laser therapy
meconium aspiration syndrome
-Presence of meconium-stained amniotic fluid suggests in utero distress with asphyxia, hypoxia, and acidosis
-Aspiration may occur in utero or -> MC -> immediately after delivery
-Meconium aspiration PNA
-Clinical Manifestations: Tachypnea, hypoxia, hypercapnia, atelectasis, small airway obstruction > air trapping, overdistention, and extra-alveolar leaks
-1-2 days: Chemical pneumonitis
-CXR: Patchy infiltrates, hyperinflation, high incidence of air leaks
-Treatment: Supportive care, ventilation; surfactant therapy, inhaled nitric oxide, ECMO
persistent pulmonary HTN of the newborn
-Severe hypoxemia w/o evidence of parenchymal lung or structural heart disease
-Often with asphyxia or meconium-stained fluid
-R to L shunting through a patent FO, PDA, and intrapulmonary channels
-Dx: Confirmed via echo –> elevated pulmonary artery pressures and sites of R to L shunting
-Tx:
-Supportive care, assisted ventilation; inhaled nitric oxide, pulmonary artery vasodilating agent; ECMO
neonatal anemia
-Symptomatic anemia may be caused by decreased RBC production (bone marrow failure, infection, congenital anemia), increased RBC destruction (MC), or blood loss
-Increased RBC Destruction (immune and non-immune causes):
-Immunologically mediated hemolysis in utero may lead to erythroblastosis fetalis (Rh incompatibility) or hemolytic ds (ABO blood group incompatibility)
-Mother has IgG antibodies from previous exposure to A or B antigens -> cross placenta and affect fetus/newborn
-Hemolytic Ds - Significant anemia and hyperbilirubinemia (MC cause of neonatal form requiring therapy)
hyperbilirubinemia: jaundice
-First day: Always pathologic and may be unconjugated or conjugated (MC)
-Early onset usually result of hemolysis, internal hemorrhage, or infection
-> 2 weeks of age: Pathologic and suggests direct hyperbilirubinemia
-Physical evidence: Observed in infants when bilirubin levels reach 5-10 mg/dL
-Lab evaluation: Total bilirubin (possible breakdown), blood typing, Coombs test, CBC, blood smear, and reticulocyte count
indirect/unconjugated hyperbilirubinemia (know this)
-Physiologic Jaundice (dx of exclusion) – 2-3 days after birth
-Result from normal physiologic characteristics of newborns: Increased RBC mass, shortened RBC lifespan, hepatic immaturity
-indirect, unconjugated
-Peak, indirect bilirubin level of no more than 12 mg/dL on day 3 of life
-Breast-feeding Jaundice (first several days)
-Due to decreased fluid intake
-Breast Milk Jaundice (first - 2nd week of life)
-Breast milk may contain inhibitor of bilirubin conjugation or may increase enterohepatic recirculation of bilirubin
-Crigler-Najjar Syndrome: Serious, rare, autosomal recessive, permanent deficiency of glucoronosyl transferase (conjugation enzyme)
-Gilbert Disease: Mutation of glucoronosyl transferase
therapy of indirect hyperbilirubinemia
-Phototherapy: Blue/white lights to reduce bilirubin levels
-Transforms bilirubin into water-soluble isomers
-Exchange transfusion
-Level of 20 mg/dL of indirect-reacting bilirubin (infants > 2000 grams)
-Umbilical venous catheter placed in IVC/umbilical vein/portal system
kernicterus spectrum disorder (bilirubin encephalopathy)
-when indirect bilirubin is deposited in brain and disrupts neuronal metabolism and function (crosses BBB due to being lipid soluble)
-Serum bilirubin > 25 mg/dL
-Earliest sx (4 days of life): Lethargy, hypotonia, irritability, poor Moro response, poor feeding
-Late sx: Bulging fontanel, pulmonary hemorrhage, fever, hypertonicity, paralysis of upward gaze, seizures
-Treatment: Immediate exchange transfusion
direct/conjugated hyperbilirubinemia
-Never physiologic
-not neurotoxic, signifies serious underlying disorder involving cholestasis or hepatocellular injury
-Labs: LFTs, bacterial/viral cultures, sweat chloride test, liver bx
-Treatment:
-Treat the cause
-Does NOT respond to phototherapy or exchange transfusion
necrotizing enterocolitis
-MC intestinal emergency in preterm infants (< 34 wks who have been fed enterally) admitted to NICU
-Intestinal involvement ranges from mucosal damage to perforation
-Prematurity assoc with immaturity of GI tract, decreased integrity of mucosal barrier, depressed mucosal enzymes, suppressed GI hormones, suppressed intestinal motility, and differences in blood flow autoregulation
-Feeding with human milk/probiotics has shown to have a beneficial role in reducing the incidence of NEC vs formula
-Early sx: Abdominal distention, feeding intolerance/increased gastric residuals, emesis, rectal bleeding, and occasional diarrhea
-Late sx: Severe distention, bilious emesis, abdominal wall erythema, lethargy, temp instability, apnea/bradycardia, DIC, shock
necrotizing enterocolitis: dx and tx
-Imaging: Intestinal ileus (obstruction), thickening of bowel loops, air-fluid levels
-Pathognomonic finding: Pneumatosis intestinalis!! -> bacteria producing gas
-Management
-D/C of enteral feedings (wont move through), GI decompression w/ NG suction, fluid/electrolyte replacement, TPN, and systemic broad- spectrum antibiotics
-Surgery when presence of pneumoperitoneum is observed on AXR – laparotomy with removal of necrotic, nonviable bowel
sepsis and meningitis epidemiology
-sepsis: approx 1:1500 in term infants and 1:250 in preterm infants (immature immunologic system and prolonged periods of hospitalization)
-Preterm infants < 32 weeks have not received full complement of maternal antibodies
-most likely meningitis
-meningitis: approx 1 in 20 cases of sepsis
-Causative agents: Same as those in neonatal sepsis
-Early-onset sepsis (birth – 7 days) sx, dx, tx
-dont know details
-Early-onset sepsis (birth – 7 days)
-Begins in utero and usually the result of infection from bacteria in moms GU tract
-Risk factors: Vaginal infection, PROM, amnionitis, maternal fever/leukocytosis, fetal tachycardia, preterm birth
-Group B streptococci!!!!!!, E. coli, Klebsiella, L. monocytogenes, and non-typeable H. influenzae
-Multi-organ disease: Respiratory failure, shock, meningitis (30% of cases), DIC, acute kidney injury, peripheral gangrene
-Work-up: Blood and CSF cultures, CSF gram stain, cell count, and protein/glucose levels; CXR to r/o PNA; ABG to detect hypoxemia/metabolic acidosis; BP, UOP, peripheral perfusion checked for shock
-Treatment:
-Immediate antibiotic therapy + assisted ventilation/cardiovascular support
-Ampicillin + aminoglycoside (gentamicin) x 10-14 days (if meningitis x 21 days)
late onset sepsis (8-24 days)
-Healthy, term infant, discharged in good health from nursery
-Similar pathogens to early-onset sepsis; also H. influenzae, S. pneumoniae, and Neisseria meningitides); viral agents as well (HSV, CMV, enteroviruses)
-Manifestations: Lethargy, poor feeding, hypotonia, apathy, seizures, bulging fontanel, fever, and direct-reacting hyperbilirubinemia
-Work-up similar to that of infants with early-onset sepsis; attention to physical exam, bone exam (rule out osteomyelitis) and urine culture
-Treatment similar to early-onset sepsis
congenital infections: toxoplasmosis
-Hydrocephalus, chorioretinitis, and intracerebral calcifications
-Infants tend to be SGA, develop early-onset jaundice, hepatosplenomegaly, and generalized maculopapular rash; seizures are common, skull films > diffuse cortical calcifications
-Diagnosis: Serologic testing
-Treatment: Pyrimethamine (supplement with folic acid) + sulfadiazine, up to 1 year
congenital infections: rubella
-MC abnormalities
-Ophthalmologic: Cataracts, retinopathy, glaucoma
-Cardiac: PDA, peripheral pulmonary artery stenosis
-Auditory: Sensorineural hearing loss
-Neurologic: Behavioral disorders, meningoencephalitis, developmental delay
-Diagnosis: Serologic testing; isolation from blood, urine, CSF, throat
congenital infections: cytomegalovirus
-MC congenital infection and leading cause of sensorineural hearing loss, intellectual disability, retinal disease, and cerebral palsy
-Microcephaly, thrombocytopenia, hepatosplenomegaly, hepatitis, intracranial calcifications, chorioretinitis, and hearing abnormalities
-Diagnosis: Detection of virus in urine or saliva
-Treatment: Ganciclovir has shown positive effect on hearing loss
congenital infections: herpes simplex
-Symptoms develop 5-10 days of life: Disseminated infection (liver, lungs, possibly CNS)
-Diagnosis: Sampling from skin vesicle, NP, eyes, urine, blood, CSF, stool, rectum (PCR)
-Treatment: Acyclovir (parenteral)
congenital infections: syphilis
-Symptoms vary: Hepatosplenomegaly, snuffles, lymphadenopathy, mucocutaneous lesions, osteochondritis, rash, hemolytic anemia, and thrombocytopenia
-Later symptoms in untreated: !Hutchinson triad! - Interstitial keratitis, CN VIII deafness, Hutchinson teeth
-Bowing of the shins, frontal bossing, mulberry molars, saddle nose, rhagades, and Clutton joints
-More than 90% of infants show XR abnormalities of long bones consistent with osteochondritis/perichondritis
-Diagnosis
-Dark-field examination of direct fluorescent antibody staining of organisms obtained by scraping of a skin or mucous membrane lesion
-Serologic testing (VDRL/RPR)
-CSF should be examined as well
-Increased WBC count + protein concentration suggest neurosyphilis
-+ CSF VDRL is diagnostic
-Treatment: Penicillin (parenteral) x 10-14 days, repeat titers at 3, 6, 12, months (neurosyphilis q 6 months x 3 years)
gonorrhea
-MC infection of eyes – ophthalmia neonatorum (first 5 days of life)
-Hyperacute onset of mucopurulent conjunctivitis
-Treatment: IM ceftriaxone x 1
chlamydia
-MC infection site is the nasopharynx; also, conjunctivitis (25-50%) and/or PNA (5-20%)
-Conjunctivitis: 5-14 days of life x 1-2 weeks, mucopurulent conjunctivitis
-Diagnosis: Culture discharge, Giemsa staining of conjunctival scrapings (diagnostic), PCR
-Treatment: Azithromycin (PO) x 3 days or erythromycin x 14 days
zika virus
-Arthropod-borne flavivirus transmitted by mosquitos
-Transmitted to fetal brain; may also lead to craniofacial abnormalities, pulmonary hypoplasia, and contractures
-Microcephaly, cerebellar hypoplasia, ventriculomegaly, lissencephaly
neonatal drug withdrawal: opiates
-Infants may become passively and physiologically addicted to medications or drugs of abuse taken chronically by mother during pregnancy – exhibit withdrawal symptoms over time
-Opiates
-Neonatal Abstinence Syndrome: Heroin onset 1-5 days, methadone onset 1-4 weeks
-Clinical Manifestations: Sneezing, yawning, ravenous appetite, emesis, diarrhea, fever, diaphoresis, tachypnea, high-pitched cry, tremors, jitteriness, poor feeding, seizures
-Treatment
Initially, swaddling in blankets in a quiet, dark room
Medications: Opioids are first-line (weaned over 1-2 months), phenobarbital for seizure withdrawal
neonatal drug withdrawal: cocaine
-Neonatal irritability, inattentiveness
-May be SGA, small head circumference
-Usually, no treatment needed
