Birth Trauma & Newborn Disorders Flashcards
What is Caput
Edema that crosses suture lines, soft, resolves in a few days
What is cephalohematoma?
Blood between skull & periostem
Does not cross suture lines, firm and defined
Resolves over 2-3 weeks
Hemolysis of RBCs = increased risk of hyperbilirubinemia
Linear skull birth trauma
Most common, not unusual with cephalohematoma, no treatment
Depressed skull birth trauma
“Ping pong ball” indention
CT to evaluate for underlying trauma to brain
Clavicle birth trauma
Most common birth fracture
Increased risk with macrosomia, breech delivery
Signs: limited arm (unilateral) movement and absense of moro reflex on affected side, crepitus over clavicle
No treatment- comfort measures
Facial birth trauma of peripheral nervous system
Increased risk with forceps delivery or prolonged 2nd stage
Typically self-limiting, resolves within hours or days
Protect cornea, assist with feeding
Brachial plexus trauma
Most common birth related paralysis- mechanical trama to spinal nerve roots at c5-T1
Presentation: arm hangs at side, shoulder adducted and internally rotated, wrist and fingers flexed, grasp reflex typically present, absent moro reflex on affect side
Treatment: immobilization and ROM, resolves in most infants, surgery rarely indicated
Intracranial hemorrhage: subdural
Risk factors: difficult or precipitous delivery, assisted birth, LGA
Intracranial hemorrhage: subarachnoid
Risk factors:
full term: trauma
preterm: hypoxia
Infants of diabetic mothers: macrosomia
Increased birth trauma
Increased hypoglycemia
Increased hypocalcemia
Increased hyperviscosity
Increased hyperbilirubinemia
Infants of diabetic mothers: respiratory distress
Increased risk if born <38 weeks
Increased maternal hyperglycemia = decreased fetal lung maturity
-impaired surfactant synthesis: increased fetal glucose, increased fetal insulin
Infants of diabetic mothers: hypoglycemia causes
increased maternal glucose = increased fetal insulin production
After birth decreased available circulating glucose but still increased fetal insulin = hypoglycemia
Infant hypoglycemia S/S
Jittery
Weak cry
Apnea or tachypnea
Hypotonic, decreased activity
If severe could lead to seizures
Infant hypoglycemia management
Prevent with early frequent feeds - most common in 1st 1-6 hours
monitor blood sugars - ideally >40-45
IV dextrose if unable to feed or symptomatic or blood sugar <25
Keep warm
Infants of diabetic mothers: hyperbilirubinemia patho
Increased insulin –>
Increased metabolic rate –>
Increased ox demand –>
Increased RBC production =
Polycythemia =
Increased hemolysis
Hyperbilirubinemia management
Early frequent feeds: feed in first 1-2 hours then 8-12 times/24 hrs, lactation consultation early if feeding difficulties
Assess for jaundice every 8-12 hrs
If jaundice <24 hrs check transcutaneous or serum bili and follow nomogram
Otherwise predischarge screening
Phototherapy prn
Neonatal sepsis classifications
Congenital
Early onset
Late onset
Neonatal sepsis S/S
Irritable, lethargic
Poor feeding
Temperature instability
Respiratory distress, apnea, cyanosis
Jaundice
Seizures
Abnormal bleeding
Neonatal sepsis treatment/prevention
Best intervention is prevention: antenatal maternal screening, eye prophylaxis, sterile/aseptic procedures, hand hygiene, avoid sick contacts
Collect specimen- blood, urine, stool
IV fluids
Oxygen
IV antibiotics/antifungals/antivirals - possible isolation
Comfort
Infection: Group B Streptococcus (GBS)
Prenatal assessment and prevention is key
-all women screened at 36 0/7-37 6/7 weeks
–>if positive treat with intrapartum antibiotic prophylaxis: PCN or ampicillin
-if presents in labor before GBS screening or no prenatal care follow algorithm
Gonorrhea
Eye prophylaxis with erythromycin ointment to prevent opthalmia neonatorium
Syphilis
Congenital syphilis rate increaseing- associated with SAB/stillbirth, early infant death if no maternal treatment
Mother should be treated with PCN G to prevent placental transmission
HIV
Rare to be symptomatic at birth
25% chance of transmission if mom untreated
All infants born to seropositive moms presumed positive
Bathe ASAP
Prompt antiretroviral administration within 12 hours of birth to slow the progression
Breastfeeding is contraindicated
Intrauterine risk of tobacco
SAB
Placental abruption and placenta previa
SGA, LBW infant, preterm birth
Extrauterine risks of tobacco
Ear infections
Chronic respiratory infections
SIDS
Patient teaching of tobacco
Smoking cessation
No smoking around infant
Fetal Alcohol Syndrome
- Dysmorphic facial features: small eyelids fissures, thin upper lip, missing vertical groove in median portion of upper lip
- Growth deficiency: pre & postnatal, IUGR, LBW, short birth length, <10th percentile
- CNS abnormalities (structural, developmental & functional): microcephaly, low cognitive functioning, attention or hyperactivity, poor social & language skills
Opioids/Neonatal Abstinence Syndrome (NAS) Manifestations
- CNS Dysfunction
- tremors
-generalized seizures
-hyperactive reflexes
-irritability
-hypertonic muscle tone, constant movement
-shrill, high-pitched cry
-disturbed sleep patterns - Metabolic, Vasomotor, and Respiratory Disturbances
-fever
-frequent yawning
-mottling of the skin
-sweating
-nasal stuffiness
-temperature instability
-frequent sneezing - Gastrointestinal dysfunction
-poor feeding
-frantic sucking or rooting
-uncoordinated sucking
-poor weight gain
-loose or watery stools
-regurgitation or projectile vomiting
RH incompatibility
Rh - mom and Rh + fetus
Sensitization: fetal RBCs with Rh antigens pass through placenta to maternal circulation causing maternal antibody production
Affect on fetus = relative number of antibodies produced, increased antibodies increased destruction of fetal RBCs –> anemia/hyperbilirubinemia
Most cases mild resulting in little to no anemia or hyperbilirubinemia
Prenatal RH incompatibility
Indirect Coombs test on mom
If + check antibodies q 2-4 weeks
At birth Rh incompatibility
Direct Coombs on fetal cord blood
If + follow H&H and bilirubin more closely, ensure early and frequent feeds, avoid stressors
Treatment of Rh incompatibility
phototherapy for hyperbilirubinemia, if severe exchange transfusion
Severe Rh incompatibility
Erythroblastosis fetalis- excessive fetal RBC (hemolysis) and fetal hyperbilirubinemia
Hydrops fetalis- severe hemolytic anemia with fetal cardiac decompensation, hepatomegaly, edema
ABO incompatibility
Most common cause of hemolytic dz in the newborn: pathologic hyperbilirubinemia
Fetal blood type A, B, AB and mom O
Maternal anti- A and anti- B antibodies are transferred across placenta from mom to baby
Anemia: mild if occurs
Hyperbilirubinemia: typically resolved with phototherapy, exchange transfusion is rare
Cardiac congenital anomalies
Most common congenital anomaly
Often associated with anomalies of other systems or chromosomal abnormalities
S/S of cardiac congenital anomalies
Central cyanosis, pallor at birth
Cyanosis or pallor with crying or feeding
Lethargy
Irregular HR
Murmur
Bonding pulses, decreased capillary refill, >20mmHG difference in BP between upper and lower extremities
Tachypnea
Nursing actions cardiac congenital anomalies
Modify feeds to reduce energy expenditure
Elevate head and shoulders to reduce cardiac workload
Knee-chest if respiratory distress
Newborn CCHD Screening
24-48 hrs of life
Pulse ox
Preductal (r. hand)
Postductal (L or R. foot)
Pass: SpO2 > or = 95% in hand OR foot AND hand-foot difference < or = 3%
Nursing actions of meningocele & myelomeningcele CNS congenital anomalies
Prone positioning
Sterile dressing and plastic to prevent drying of exposed defects
Reduce infection risk- diaper care
Head circumference
NO LATEX
Choanal Atresia
Blockage of posterior nares
Infants are obligate nose breathers first 4-6 weeks of life
Respiratory distress, decreased SaO2, cyanosis at rest, feeding, or pacifier use
With cry, color, SaO2 improve and distress resolves
Congenital diaphragmatic hernia
Often diagnosed with prenatal ultrasound
Commonly associated with chromosomal abnormalities or defects of cardiac and MSK systems, male > female
Severity of symptoms depends on size of defect
-large defects associated with significant respiratory distress at birth, cyanosis, mottling, pulmonary hypertension
Cleft Lip/Palate
Genetic and environmental
Mild to severe
Cosmetic and functional
Risk for compromised airway, feeding, speech development
Omphalocele
Covered herniation of abdominal contents into base of umbilical cord
Gastroschisis
Herniation of abdominal contents through defect in abdominal wall with no covering membrane
Nursing care of omphalocele/gastroschisis
Sterile moist dressing over defect, polyethylene bag over torso
Side lying
Replogle gastric tube for decompression
Thermoregulation, fluid balance, infection risk reduction
Esophageal atresia & Tracheoesophageal fistula
Esophagus with a blind pouch (dead end) and/or fistula to trachea
Infants with excessive oral secretions, drooling, respiratory distress and feeding intolerance are suspicious for TEF
-do not feed orally and notify provider
Raise HOB, replogle to LIS, anti-reflex/antacid meds
Surgical intervention
Four components of congenital clubfoot
- inversion and adduction of the forefoot
- inversion of heel and hindfoot
- limitation of extension of the ankle
- internal rotation of the leg
Ponseti method for clubfoot
Stretching and casting
Move infant’s foot into a correct position and then place it in a cast to hold it there
Reposition and recast the infant’s foot once a week for several months
Possibly a minor surgical procedure to lengthen the Achilles tendon toward the end of this process
Congenital hip dysplasia
Hip joint laxity
Demonstrated with Barlow and Ortolani maneuvers during newborn assessment but most reliable at 2-3 months
Hip dysplasia treatments
Infants are usually treated with a soft brace, such as a Pavlik harness, that holds the ball portion of the joint firmly in its socket for several months. This helps the socket mold to the shape of the ball
Double diapering is no longer recommended as interferes with proper hip development
Hypospadias
Abnormally located urinary meatus on the underside of the penis
Increased severity results in urinary and infertility problems
Surgery at approx 6 months
Epispadias
Urethra opening at the top or side of the penis
Often occurs with exstrophy of the bladder
Bladder exstrophy
Prevent infection (cover)
Preserve renal fxn
Maintain skin integrity
Ambiguous genitalia
Discrepancy between the chromosomal sex and external genitalia
External genitalia anatomy is unclear
Karyotyping
Counseling
Phenylkeonuria (PKU)
Genetic disorder caused by a deficiency of the liver enzyme, phenylalanine hydroxylase
Results in increased levels of amino acid phenylalanine leads to CNS damage which leads to intellectual disability
Symptoms of PKU
Vomiting
Poor feeding
FTT
Overactivity
Irritability
Musty-smelling urine
Treatment of PKU
Lifelong low protein diet- special infant formula without phenylalanine
Breastfeeding only in conjunction with phenylalanine free formula
Galactosemia
Genetic disorder resulting in deficiency of enzyme that convert galactose to glucose
Early symptoms of galactosemia
Vomiting, poor weight gain
Hypoglycemia
Liver damage, hyperbilirubinemia
Frequent infections
CaTaracts
Treatment of galactosemia
Lifelong galactose free diet and calcium supplementation
Breastfeeding is contraindicated due to presence of. lactose
Congenital hypothyroidism
Multiple causes: defects with thyroid gland and/or thyroid hormone –> decreased levels of T4 & elevated levels of TSH
Ideally screen at 3 days of life and repeat at 2 weeks of age
Symptoms of congenital hypothyroidism
Large protruding tongue, distended abdomen, constipation, poor feeding
Slow reflexes
Large, open posterior fontanelle
Hypothermia
Hoarse cry
Dry skin, coarse hair
Goiter, jaundice
Treatment of congenital hypothyroidism
Untreated: irreversible cognitive & motor impairment
Treatment: lifelong thyroid replacement hormone
