1 Flashcards
mom received meperidine (Demerol) and phenargan during labor due to inadequate spinal anesthesia and baby is blue, floppy and poorly responsive, what to do?
- initiate positive-pressure ventilation (PPV) by bag and mask
- naloxone (Narcan IV, IM, SQ or endotracheal) administration may transiently reverse the effect of the narcotic (meperidine), which is likely the cause of the neonatal respiratory depression (narcosis)
The 1-minute Apgar score helps to determine an infant’s well-being in the period just prior to delivery, and scores ? historically have been used to indicate the need for immediate resuscitation
less than 3
-the 5-minute score is one indicator of how successful the resuscitation efforts were
A child presents with immediate respiratory distress, scaphoid abdomen, cyanosis, and heart sounds displaced to the right side of the chest, think what condition?
how to manage?
diaphragmatic hernia
- will often have pulmonary hypoplasia, endotracheal intubation is the best course of action
- Bag-and-mask ventilation will cause accumulation of bowel gas (which is located in the chest) and further respiratory compromise.
Choanal atresia results in respiratory distress when a child stops crying; immediate treatment is ?
intubation until surgical correction can be completed
if neonatal HR is still less than 60 beats/min despite positive-pressure ventilation (PPV) with 100% oxygen, what next step?
if HR still less than 60 what next?
give chest compressions for 30 seconds
If the HR is still less than 60 beats/min, then drug therapy (usually epinephrine) is indicated.
causes of tachypnea in the IDM (infant of diabetic mother)
*hypoglycemia, RDS, HCM, hypocalcemia, polycythemia, and clavicle fracture
fetal hyperinsulinism begins in the second trimester resulting in ?
fetal macrosomia and increased fetal oxygen requirements
Maternal hyperglycemia very early in gestation can cause ?
NTDs and congenital heart disease
Fetal insulin production causes increased glycogen production deposited in fetal liver, heart, kidneys, muscles..leads to complications such as
difficult delivery, HCM, polycythemia due to incr. O2 requirements, RDS due to insulin interfering with cortisol’s ability to induce surfactant production
hypoglycemia is a blood sugar less than ?
symptoms?
less than 40 mg/dL
lethargy, listlessness, poor feeding, temperature instability, apnea, cyanosis, jitteriness, tremors, seizure activity, respiratory distress, hypothermia (vomiting is NOT a symptom)
macrosomia defined
Larger than normal baby with the birth weight exceeding the 90th percentile for gestational age, or any birth weight more than 4 kg.
If hyperglycemia is present in the first trimester, an increased risk for congenital anomalies of ?
the CNS, heart, kidneys, and skeletal system (such as caudal regression syndrome in which there is hypoplasia of the sacrum and lower extremities)
a neonate with a blood glucose level of less than 40 mg/dL with any symptom of hypoglycemia requires ?
If no symptoms of hypoglycemia are present what to do?
IV glucose
the infant is refed and the glucose is remeasured 30 minutes after the feeding.
what is a metabolic abnormality commonly seen in IDM and presents as irritability, sweating, or seizures
hypocalcemia, treat with IV calcium
how does polycythemia (HCT more than 65) develop in a macrosomic neonate and how does it present
Macrosomia in utero increases O2 requirement, and the relative placental insufficiency leads to increased production of EPO
-may give a ruddy or plethoric hue to the infant’s skin
Polycythemia contributes to elevated ? levels
can cause?
how to treat?
bilirubin
hyperviscosity syndrome with resultant venous thrombosis in the renal veins, cerebral venous sinus, or mesenteric veins
treated with increased hydration and in rare instances partial exchange transfusion
Neonatal hyperbilirubinemia appears when ? results from higher rates of ? and a limited ?
first week of life bilirubin production (RBCs are lysed at too rapid a rate)
limited ability to excrete it (ie, transmission of unconjugated bilirubin to the liver is interrupted; liver enzyme deficiencies preclude appropriate metabolism of the unconjugated material)
risk factors for neonatal jaundice
male gender, cephalohematoma, Asian ancestry, breast-feeding, maternal DM, prematurity, polycythemia, trisomy 21, delayed bowel movement, upper GI obstruction, hypothyroidism, swallowed maternal blood, and a sibling with physiologic jaundice.
Unconjugated or Indirect Hyperbilirubinemia ddx
Hemolytic disease (ABO, Rh, or other minor blood group incompatibility), Structural/metabolic abnormalities of RBCs (hereditary spherocytosis, G6PD deficiency), Hereditary defects in bilirubin conjugation (Crigler-Najjar—Types I and II, Gilbert disease) Bacterial sepsis, Breast milk jaundice, Physiologic jaundice
Conjugated or Direct Hyperbilirubinemia ddx
Conjugated biliary atresia, Extrahepatic biliary obstruction, Neonatal hepatitis (Bac, Viral, Nonspecific, TPN related), Short bowel related, Inspissated bile syndrome, Postasphyxia, α1-Antitrypsin deficiency, Neonatal hemosiderosis
does conjugated or unconjugated bilirubin cause neurotoxicity?
unconjugated (conjugated cannot cross BBB)
Clinical and laboratory findings of hemolysis
rapid rise of serum bilirubin level (more than 0.5 mg/dL/h), anemia, pallor, reticulocytosis, and hepatosplenomegaly.
kernicterus is a neurologic syndrome resulting from unconjugated bilirubin deposition in brain cells, especially the ? Less mature or sick infants have greater susceptibility. common initial signs ?
basal ganglia, globus pallidus, putamen, and caudate nuclei
Lethargy, poor feeding, and loss of Moro reflex
ETCO
END-TIDAL CO CONCENTRATION corrected for ambient CO; provides a noninvasive assessment of bilirubin production.
TRANSCUTANEOUS BILIRUBINOMETER (TcB):
device that is placed on infant’s skin and produces light at several wavelengths that then measures its reflection after interacting with the serum bilirubin in the microcirculation beneath the skin. used as alternative to blood test to noninvasively measure serum bilirubin
Jaundice usually begins on the ? and then progresses to the ? Full-term newborns with physiologic jaundice usually have peak bilirubin concentrations of ? between the second and fourth days of life
face and then progresses to the chest, abdomen, and feet.
5 to 6 mg/dL
Findings suggestive of nonphysiologic jaundice
(1) appearance in the first 24 to 36 hours of life
(2) bilirubin rate of rise greater than 5 mg/dL/24 h
(3) bilirubin greater than 12 mg/dL in a full-term infant without other physiologic jaundice risk factors listed
(4) jaundice that persists after 10 to 14 days of life
Causes of nonphysiologic jaundice
septicemia, biliary atresia, hepatitis, galactosemia, hypothyroidism, cystic fibrosis, congenital hemolytic anemia (eg, spherocytosis, maternal Rh, or blood type sensitization), or drug-induced hemolytic anemia
jaundice presenting within the first 24 hours of life requires immediate attention; causes include ?
erythroblastosis fetalis, hemorrhage, sepsis, cytomegalic inclusion disease, rubella, and congenital toxoplasmosis
Significant hyperbilirubinemia requires a diagnostic evaluation
indirect and direct bilirubin concentrations, Hgb level, reticulocyte count, blood type, Coombs test, and peripheral blood smear examination.
commonly used treatment for unconjugated hyperbilirubinemia
phototherapy: light converts the skin’s bilirubin isomerization into a more easily excreted form
Exchange transfusion is needed in a small number of jaundiced infants who do not respond to conservative measures, what does it involve?
Small aliquots of the infant’s blood are removed via a blood vessel catheter and replaced with similar aliquots of donor blood
risks of exchange transfusion
air embolus, volume imbalance, arrhythmias, acidosis, respiratory distress, electrolyte imbalance, anemia or polycythemia, blood pressure fluctuation, infection, and necrotizing enterocolitis.
maternal ingestion of ? during pregnancy decreases the risk of neurologic damage in a jaundiced newborn
phenobarbital, as it induces glucuronyl transferase (UGT), thus reducing neonatal jaundice
Crigler-Najjar syndrome
Severe deficiency of uridine diphosphate glucuronosyltransferase
type I have a severe deficiency, causing high bilirubin levels and encephalopathy. Treatment is phototherapy. Encephalopathy is rare with Crigler-Najjar syndrome type II, in which bilirubin levels rarely exceed 20 mg/dL.
early-onset neonatal sepsis
1st 6 days of life, 85% in 1st day, , orgs from mom’s GU tract: GBS, E coli, H influenzae, and L monocytogenes, presents with pneumonia and sepsis
late-onset neonatal sepsis
after 7 days, before 90 days, orgs from environment
Examination findings seen frequently with pneumonia (more commonly seen in early-onset disease)
tachypnea, grunting, nasal flaring, retractions (costal or substernal), decreased breath sounds, and cyanosis
findings common in sepsis and meningitis
Temperature instability, tachypnea, hypotension, and bradycardia, poor feeding, hypoglycemia
Overwhelming shock is manifested as
pallor and poor capillary refill.
think early-onset GBS (rather than noninfectious etiology of lung problems) if
PROM, apnea, hypotension in the first 24 hours of life, a 1-minute Apgar score less than 5, and rapid progression of pulmonary disease
Factors associated with increased risk for early-onset GBS disease
ROM more than 18 hours before delivery, chorioamnionitis or intrapartum temperature greater than 100.4°F (38°C), previous infant with GBS infection, mother younger than 20 years, and LBW or prematurity (less than 37 weeks of gestation)
manifestations of late-onset GBS
bacteremia without a focus, meningitis, pneumonia, septic arthritis, osteomyelitis, or cellulitis
treatment of neonatal sepsis?
if GBS is isolated as the sole pathogen, narrow to ?
IV gentamycin/tobramycin and ampicillin for 48-72 hrs
stop if cultures are negative and pt is well
if s/s of sepsis and negative cx, continue abx
if + cx, may continue for 10-21 days
others: 1st/2nd gen cephs, vanc
IV penicillin G
hermaphroditism
Discrepancy between gonad morphology and external genitalia
Think CAH in an infant with ambiguous genitalia and these symptoms
failure to thrive (failure to regain birth weight, progressive weight loss), vomiting, and dehydration
interventions for CAH infant
fluid resuscitation, electrolyte repletion, adrenocorticoid replacement (hydrocortisone helps to inhibit excessive production of androgens and further virilization)
an important first step in the laboratory evaluation of infants with ambiguous genitalia
Karyotype analysis using activated lymphocytes
If CAH is suspected, biochemical markers might include an elevated ?
serum 17-hydroxyprogesterone level
how to determine whether a block in testosterone synthesis or 5a-reductase deficiency exists
measure urinary steroids and plasma androgens before and after administration of ACTH and hCG
other studies for ambiguous genitalia
ultrasonogram or pelvic MRI, urogenital sinus x-ray after contrast injection, and fiberoptic endoscopy
typically NOT laparascopy
what condition has functional testicular tissue, with normal or high testosterone levels, have 46,XY karyotypes, yet appear as phenotypically normal females with short or atretic vaginas
testicular feminization
