exam 1 - neonatal Flashcards

1
Q

fetus and newborn

A

-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

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2
Q

maternal risk factors

A

-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)

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3
Q

fetal to neonatal physiology transition

A

-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!

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4
Q

routine delivery room care: Apgar score

A

-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

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5
Q

routine delivery room care

A

-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

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6
Q

delivery room resuscitation

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-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

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7
Q

delivery room resuscitation: asphyxia

A

-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

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8
Q

delivery room resuscitation: shock

A

-Pallor, poor cap refill time, lack of palpable pulses, hypotonia, cyanosis, and eventually cardiopulmonary arrest
-MC cause 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

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9
Q

birth injuries (test)

A

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

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10
Q

birth injuries: facial nerve injury

A

-Asymmetric, crying face
-Eye does not close, nasolabial fold absent, side of mouth droops at rest

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11
Q

birth injuries: brachial plexus injury (test)

A

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

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12
Q

birth injuries: spine/spinal cord injuries

A

-If excessive force during vertex/breech delivery
-Rotational – C3-4
-Longitudinal – C7-T1
-Spinal cord: Flaccid, apneic, and asphyxiated on PE

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13
Q

birth injuries: clavicle fractures

A

-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

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14
Q

birth injuries: visceral trauma

A

-Macrosomic, extremely premature infants
-Liver rupture: Anemia, hypovolemia, shock, hemoperitoneum, and DIC
-Adrenal rupture: Flank mass, jaundice, hematuria

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15
Q

newborn hernias

A

gastroschisis:
-Herniation of bowel through abdominal wall 2-3 cm lateral to the umbilicus
-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

omphalitis:
-Erythema around umbilicus
- may cause portal vein thrombophlebitis and subsequent extrahepatic portal HTN)
-know the picture and difference

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16
Q

PE of newborn: genitalia

A

-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

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17
Q

respiratory distress syndrome (hyaline membrane disease)

A

-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

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18
Q

respiratory distress syndrome (Hyaline Membrane disease): clinical manifestation

A

-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

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19
Q

respiratory distress syndrome (Hyaline Membrane disease): complications: PDA

A

-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

20
Q

respiratory distress syndrome (Hyaline Membrane disease): complications: pulmonary air leaks

A

-Assisted ventilation may cause overdistention of alveoli > rupture > interstitial emphysema > PTX/pneumomediastinum
-Confirmed by CXR
-Treatment: Symptomatic PTX > pleural chest tube

21
Q

respiratory distress syndrome (Hyaline Membrane disease): complications: bronchopulmonary dysplasia (chronic lung ds)

A

-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

22
Q

respiratory distress syndrome (Hyaline Membrane disease): complications: retinopathy of prematurity (retrolental fibroplasia)

A

-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

23
Q

meconium aspiration syndrome

A

-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

24
Q

persistent pulmonary HTN of the newborn

A

-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

25
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)
26
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
27
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
28
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
29
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
30
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
31
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
32
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
33
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
34
-Early-onset sepsis (birth – 7 days) sx, dx, tx -dont know details
-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)
35
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
36
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
37
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
38
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
39
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)
40
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)
41
gonorrhea
-MC infection of eyes – ophthalmia neonatorum (first 5 days of life) -Hyperacute onset of mucopurulent conjunctivitis -Treatment: IM ceftriaxone x 1
42
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
43
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
44
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
45
neonatal drug withdrawal: cocaine
-Neonatal irritability, inattentiveness -May be SGA, small head circumference -Usually, no treatment needed