perinatal care triggers Flashcards
Early first-trimester insults like chromosomal or congenital abnormalities, resulting in global growth delay
this is the primary cause of what?
fetal grwoth restriction (FGR) and IUGR
what mechanism causes the closure of the PFO
Increased O2 in blood –> increased blood flow in lungs —> increased venous return to LA —> LA pressure increase closes PFO
what aids babies in learning to regulate their temperature and also helps moms milk production
skin to skin in the golden hour after birth
what ceases low-resistane circuit in the placenta and also increases systemic BP and relaxes lung vessels for a baby
clamping of the umbilical cord
Apnea/gasping & HR < 100 BPM indicates what should be done
PPV via BVM at 40-60 breaths per minute
when do we use MR SOPA
when PPV does not seem to be working properly
while doing MR SOPA place baby on SPO2 moniter and continuous EKG.
if the heart rate is <60 despite 30s of PPV what is the next step
intubate.
compressions recommended for resuscitation.
3:1 compressions for 90 compressions and 30 breaths.
consider umbilical vein catheterization
when should epinephrine be considered
if HR <60
(im assuming after youve tried PPV and compressions)
when should we examine for hypoxic ischemic encephalopathy or therapeutic hypothermia
if a newborn >= 36 weeks received resuscitation
Delayed resorption of lung fluid leading to pulmonary edema leading to tachypnea
TTN
CXR shows pleural effusions, perihilar densities with fissure fluids and hyperexpansion of the lungs
TTN
occurs in teh First 2 hours, lasting up to 72 hours but typically resolving within 12-24 hrs
TTN
respiratory distress and hypoxia triggered by uterine stress during delivery
meconium aspiration syndrome
(they just get so stressed that they poop everywhere and then inhale it)
CXR shows bilateral fluffy densities with hyperinflation of the lungs.
MAS
also diagnostic is to see meconium present in amniotic fluid or trachea during intubation
see meconium present in amniotic fluid or trachea during intubation
MAS
results in inflammation and surfactant inactivation, atelectasis, rupture of alveoli and V/Q mismatches
progression of MAS
it is NOT recommended to intubate these patients
MAS
ground glass opacities on CXR
RDS
glucocorticoids and postnatal surfactant with ventilation via NCPAP is tx for what
RDS
MC in GA>34 weeks
PPHN
associated with MAS, PNA and RDS
PPHN
this is associated with intrauterine/perinatal asphyxia as well as the exposure of fetus to SSRIs in the 2nd half of pregnancy
PPHN
presents with meconium staining, respiratory distress, and a possible harsh systolic murmur at the lower left sternal border
PPHN
echo showing normal anatomy with pulmonary HTN is diagnostic of which disease
PPHN
use nitric oxide or sildenafil in severe disease
PPHN
use ECMO as last resort
use ECMO as last resort for this disease
PPHN
risk factors include maternal exposure to labetalol or terbutaline bronchodilator, LGA, SGA, and maternal diabetes
neonatal hypoglycemia
high risk symptoms for this disease includes floppiness, exaggerated moro reflex, seizures irritability, and more
neonatal hypoglycemia
preterm babies, LGA, SGA and babies with diabetic mothers should all be screened for what
neonatal hypoglycemia
just gonna leave this right here in case anyone wants to look at it
what is pathognomonic of neonatal jandice
jaundice presenting within the first 24 hours of birth.
risk factors includes GA <38wks, albumin <3, hemolytic diseases, sepsis
neurotoxicity due to hyperbilirubinemia
what does TcB have to be for you to suspect jaundice enough to run a TSB
within 3mg/dl of the threshold or >15
What value is used as the definitive test to guide phototherapy and escalation of care decisions in jaundiced babies (including need for exchange transfusion)
TSB
what is a significant conjugated/direct bilirubin in relation to TSB
when conjugated/direct bilirubin exceeds 20% of the TSB
Fasting abd US for biliary atresia or choledochal cyst should be assessed when
when a baby has high bilirubin
caused by poor feeding, Intestinal hypomotility or poor elimination of bilirubin in stool
breastfeeding jaundice
Post 1st week of birth and lasts up to 3 wks, Inhibition of UGT and deconjugation of conjugated bilirubin
breast milk jaundice
what treatment increases an infants neurotoxicity risk factors
phototherapy during treatment of hyperbilirubinemia
feeding is considered the most important first line intervention for what diagnosis
jaundice
IV fluids is NOT recommended in combination with what therapy?
phototherapy
hypertonia of the extensor muscles such as opisthotonus and retrocollis si seen in what phase of neonatal acute bilirubin neurotoxicity
phase 2
When can we D/C phototherapy for hyperbilirubinemia?
TSB < 2 mg/dl below the hour-specific threshold
Venous Hct > 65% at term
polycythemia
Hyperviscosity of blood, resulting in decreased perfusion of the capillary beds.
polycythemia
delayed cord clamping can lead to what problem
benign neonatal polycythemia
CNS: irritability, jittery, seizures, lethargy
Cardio: respiratory distress, CHF, PPH (postpartum hemorrhage)
GI: emesis, heme-positive stool, distension
Renal: Decrease output, rena vein thrombosis
Metabolic: Hypoglycemia
Heme: Hyperbilirubinemia, thrombocytopenia
this is alot but whats it for
benign neonatal polycythemia
Isovolemic partial exchange transfusion with NS to dilute blood
but only if pt is symptomatic
benign neonatal polycythemia
amino acidopathy with a deficiency in PAH
PKU
this illness if left untreated leads to permanent brian injury due to accumulation of phe
PKU
treat by lifelong restriction of phe by eating phe - free proteins
D10 IVF given to promote anabolic state. consider hemodialysis if elevated ammonia is present.
PKU
Liver dysfunction, jaundice, and coagulopathy
E. coli sepsis and cataracts
metabolic decompensation of the infant
galactosemia
Metabolic decompensation when an infant gets formula with lactose in it.
X linked recessive
G6PD
if you test TRAbs in newborns with hypothyroidism and they are negative, what is the assumption of etiology
I think its inborn error or excess maternal iodine
may wanna lok this up becuase im only 86% sure
Protruding abdominal organs without a protective sac, almost always to the right of umbilicus
gastroschisis
Protruding abdominal organs with a protective sac
omphalocele
Usually associated with genetic anomaly/syndrome in 1/2 of cases.
omphalocele
this hernia goes straight through umbilicus
omphalocele
Elevated AFP in mothers blood may suggest what problem (not chromosomal , think physiologic developement)
omphalocele/gastroschisis and NTD
if you underestimate gestational age what lab level will be falsely elevated
AFP
Blind esophageal pouch that does not connect with esophagus/airway or connects both the esophagus and airway later.
esophageal atresia
Baby will be choking, coughing, cyanosis
esophageal atresia
TX:
Acutely: suction, elevate head, IV glucose
Definitive: Make a fistula to solve problem
esophageal atresia
fistula connects esophagus
presents with emesis after birth
upper/proximal intestinal obstruction
presents with abdominal distension, late emesis, late/no stooling in baby
distal/lower intestinal obstruction
dueodenal intestinal atresia is one of the MC intestinal atresias. what is it assocaited with
down syndrome
jejunoileal is the other MC cause and its assocaited with CF
risk factors for this is smoking and being a preemie
intestinal atresias
double bubble sign on Xray
duodenal
triple bubble sign on Xray
jejunal atresia
risk factors include inadequate folic acid, maternal DM, maternal Hyperthermia and VPA exposure
neural tube defects
missing part of the brain/skull with inability to control swallowing
ancephaly
tuft of hair on dimple
spina bifida occulta
protrusion of only the meninges
meningocele
protrusion of meninges + the spinal cord
myelomeningocele
Extremely Elevated AChesterase in amniotic fluid can confirm
NTDs
which NTD has normal AFP
spina bifida occulta
Encephalopathy due to hyperbilirubinemia (consequence of untreated jaundice)
kernicterus
