Perinatal Period Flashcards
1
Q
Gestational period:
preterm, term and post term?
A
- preterm: less than 37 wks
- term: 37-42 weeks
- post: more than 42 weeks
2
Q
Neonatal and perinatal period?
A
- neonatal: first 28 days of life (+preterm time period)
- perinatal: from 20 weeks gestation to one month after birth
3
Q
What is involved in fetal-neonate transition?
A
- cardiovascular transition
- respiratory transition
- temp maintenance
- growth transition
4
Q
3 cardiovascular shunts in the fetus?
A
- ductus venosus
- ductus arteriosus
- foramen ovale
5
Q
Ductus venosus - purpose?
A
- connects umbilical vein to IVC
- allows O2 blood directly from mom to enter circulation (bypasses liver) via IVC
- disappears within 2 weeks after birth
- becomes ligamentum venosum
6
Q
Ductus arteriosus - purpose?
What happens at birth?
A
- a channel of communication b/t the main pulmonary artery and the aorta
- allows majority of blood which would enter pulmonary vasculature to bypass directly to the aorta
- at birth: extremely sensitive to O2 content of blood, at birth increased O2 initiates constriction and subsequent closure
7
Q
Foramen ovale - purpose?
A
- opening b/t 2 atria of the fetal heart
- allows O2 blood from mom which enters right atrium to be channeled directly to left atrium (R - L shunting) - onto LV, aorta and system
8
Q
Diff in vascular resistance in uteror and at birth?
A
- in utero: systemic vascular resistance is low
pulmonary vascular resistance is high (lungs are full of fluid) - at birth: increased systemic vascular resistance, decreased pulmonary vascular resistance: this increases left atrial pressure which closes the foramen oval and eliminates R to L shunting
9
Q
What is the last system to fully mature in utero?
A
- pulmonary system
- occurs during 3rd trimester (28-40 weeks):
surfactant starts being produced, surfactant reduces surface tension and stabilizes alveoli, surfactant production is usually sufficient by 34 weeks gestation
10
Q
Temperature maintenace at birth?
A
- heat regulation isn’t well developed
- sensitivie to excess heat loss and heat retention (hypo-/hyperthermia)
- immediately after birth: dry the infant and provide radiant heat
11
Q
Growth transition after birth?
A
loss of body weight:
- occurs first few postnatal days
- wt loss of 5-10% is normal in first week after birth
- predominantly loss of extracellular water
- inadequate nutritional intake
acclimation occurs:
- most newborns back to birth wt by 2 weeks of age, feeding improves, and growth accelerates
12
Q
APGAR?
A
- Activity - 2 pt:active movement, 1: arms and legs are flexed
- Pulse - 2: over 100 bpm, 1:below 100 bpm
- Grimace - 2: active motion, 1: some flexion of extremities
- Appearance - 2: completely pink, 1: body pink, extremities blue
- Respiration - 2: vigorous cry, 1: slow, irregular
13
Q
Impt basic principles of neonatal resuscitation?
A
- O2!!!
- bulb suctioning, particularly if meconium stained amniotic fluid
- stimulation (induces sympathoadrenal mediated increases in respiratory and cardiac performance)
- drying and warming for maintenance of thermoneutrality
14
Q
Commonly screen conditions of newborn?
A
- babies born with these conditions appear completely normal, so that is why we screen!
- PKU
- galactosemia
- hemoglobinopathies
- hypothyroidism: swollen tongue, puffy face, cold extremities, low muscle tone, poor feeding, lethargic
- hearing screening
- disorders usually only develop after baby has been feeding for 2-3 days.
15
Q
What sizes is small for gestational age (SGA)?
A
- below 10th percentile on growth chart
- this is diff than intrauterine growth retardation
16
Q
What size is considered appropriate for gestational age (AGA)?
A
- b/t 10th and 90th percentile on growth chart
17
Q
What sizes are considered large for gestational age (LGA)? Most common cause of macrosomia?
A
- above 90th percentile for wt on growth chart
- macrosomia: gestational diabetes
18
Q
Symmetric IUGR?
A
- infant can be SGA due to genetics and is normal but small
- symmetric implies event in early pregnancy such as chromosomal abnormalities. drug or alcohol use, or congenital viral infections
19
Q
Asymmetric IUGR?
A
- only wt at or below 10th percentile
- head is normal size, body is smaller
- asymmetric implies problem late in pregnancy such as pregnancy induced HTN, pre-eclampsia or placental insufficiency
(better outcome)
20
Q
Causes of LGA?
A
- infant of diabetic mother
- erythroblastosis fetalis (hydrops): Rh - mom with abs with Rh + baby
-normal variants:
genetic predisposition, male fetus, post-dates gestation, and multiparity
21
Q
Why is the infant of a diabetic mother usually large for gestational age and why is the baby at risk for hypoglycemia?
A
- large because of increased amt of glucose it is receiving
- at risk for hypoglycemia because it was so used to receiving extra glucose that stimulated increase production of insulin as well - at birth not exposed to hyperglycemia - hypoglycemia state
22
Q
Why should all LGA infants be screened for hypoglycemia while in the hospital?
What are abnormal levels of glucose?
signs of hypoglycemia?
A
- b/c hypoglycemia can occur w/in 3 hrs of birth
- at 3 hrs of life normal term babies blood glucose stabilizes at 50-80 mg/dl
- concentrations below 40-45 mg/dL after first few hours of life should be considered abnormal
- heel stick to screen, if low or borderline, need direct measurement of blood
- Continued surveillance until full enteral feedings without IV supplementation for 24 hr period
- signs:
lethargy, poor feeding, irritability, termulousness, jitteriness, apnea, and seizures
23
Q
Tx of IDM hypoglycemia?
A
- IV glucose
- dose depends on level of hypoglycemia and whether there are sxs
- if infant is alert and vigorous and only mildly hypoglycemic, may just feed and monitor carefully
- ## prognosis usually excellent if therapy is prompt
24
Q
Why would IUGR infants have hypoglycemia in some cases?
A
- due to reduced glucose stores
25
Q
Normal newborn RR?
A
- 30-60
26
Q
What is respiratory distress syndrome?
A
- pulmonary system is last to fully mature
- epithelial cells in alveoli called type II cells produces surfactant
- surfactant lowers surface tension
- surfactant deficiency leads to markedly decreased lung compliance
- uncommon at 37 weeks gestation and beyond
- 70% chance of RDS at 28-30 weeks gestation
- hypoxemia and acidosis contribute to pulmonary vasoconstriction - leads to increased pulmonary vascular resistance - blood will shunt away from these areas of lungs
27
Q
Signs of RDS? What will you see on CXR?
A
- within 6 hrs of birth: tachypnea retractions nasal flaring grunting cyanosis
- on CXR:
reticulogranular pattern (ground glass)
air bronchograms
28
Q
DDx of Respiratory disorders?
A
- sepsis
- pneumonia
- pneumothorax
- mass-occupying lesions in chest (stomach herniating into chest through diaphragm)
- polycythemia
- transient tachypnea of newborn
29
Q
Management of RDS?
A
- O2 therapy with monitoring of blood gases
- CPAP
- mechanical ventilation (if needed)
- artificial surfactant replacement
30
Q
What is meconium aspiration syndrome (MAS)?
signs?
A
- staining of amniotic fluid with meconium in assoc with respiratory distress
- more common the longer the gestation (theory: fetal distress leads to meconium passage in utero followed by aspiration from gasping)
- **obstructive disease
- most common with postmaturity and fetal distress
- signs:
grunting, nasal flaring, retractions, marked tachypnea, and varying degrees of cyanosis (similar to RDS)
31
Q
What will you see on CXR, ABGs in MAS?
A
- CXR reveals fluffy infiltrates with alternating areas of lucency
- pneumothorax or pneumomediastinum and hyperinflation with flattening of diaphragm often seen
- ABGs reveal hypoxemia (low O2) and hypercarbia (high CO2) - respiratory acidosis
32
Q
Management of Meconium Aspiration Syndrome?
A
- suctioning of nose and oropharynx after delivery of the head should be done by obstetrician when meconium staining is present
- chest physiotherapy
- CPAP or mech ventilation
- routine admin of abx b/c of possible occurrence of secondary bacterial pneumonia
33
Q
What is Persistent Pulmonary HTN of newborn (PPHN)?
A
- also known as persistent fetal circulation:
pulmonary HTN, R to L shunting of desaturated blood through fetal pathways (PFO or PDA) in structurally normal heart - caused by sustained elevation in pulmonary vascular resistance
- can be idiopathic or secondary to RDS, congenitatl diaphragmatic hernia, hyperviscosity, sepsis, or other causes
- echo with color flow doppler can demonstrate R to L shunting pattern and rule out structural heart defects
34
Q
What is TTN?
What does CXR show?
A
- transient tachypnea of the newborn:
retained lung fluid
distress typically from birth
reqrs mild to mod O2 (25-50%)
-often occurs in term or near term infants - CXR shows perihilar streaking and fluid in interlobar fissures
- resolution usually occurs within 12-24 hrs
35
Q
Physiology of Jaundice:
Production and excretion
A
- jaundice is caused by excessive levels of bilirunin in the bloodstream
- porduction: bilirubin is produced from destruction of RBCs in liver and spleen
- it is unconjugated and binds to albumin and is transported to the liver
- excretion: conjugated in the liver, excreted in the biles, and eliminated in the urine and feces
- any process that causes excess destruction of RBCs or interferes with bile excretion can cause hyperbilirubinemia
- unconjugated bilirubin can pass through BBB
36
Q
Why do we care about jaundice?
A
because unconjugated (indirect) bilirubin is neurtoxic:
- bilirubin induced neuro dysfxn: BIND
- acute bilirubin encephalopathy (early signs of toxicity): neuro changes occur in first postnatal weeks, characterized by hypotonia and seizures, can be reversed unless levels of bilirubin remain elevated
- kernicterus:
chronic and permanent sequelae of BIND, develops during first year of life, can range from subtle to severe sxs
37
Q
Kernicterus? Occurs at what levels? Tx?
A
- Chronic and permanent sequelae of BIND
- can occur when unconjugated bilirubin exceeds binding capacity of albumin
- it crosses BBB to damage cells of the brain
- kernicterus can occur in full term newborns when unconjugated bilirubin levels are above 20-25 mg/dL
- occurs at lower levels with premature infants
- tx depends on circumstance and rate of bilirubin increase
38
Q
3 mechanisms that predispose newborns to physiologic jaundice?
A
- bilirubin production is higher:
newborns have higher HCT (50-60%), fetal RBCs have shorter life span and there is greater turnover of RBCs - bilirubin clearance by the liver is decreased due to decrease in enzyme - UGT1A1
- increased enterohepatic circulation: conjugated bilirubin (can’t be reabsorbed) reaches infant’s gut
- B-glucuronidase in infant’s gut acts on bilirubin to make it unconjugated and then reabsorbed into circulation again
- the infant gut has few bacteria in it to counter the effects of B-glucuronidase
39
Q
Progress of physiologic jaundice of the newborn?
A
- begins after 24 hrs of life
- peaks at level of 12-15 mg/dL of indirect bilirubin at around 3 days of life
- returns to normal by days: 10-12
- progresses cephalocaudally (head to toe)
- premature infants may take 4-5 days to reach peak bilirubin levels, and these peaks may be twice that observed among full term infants
40
Q
At what serum bilirubin level does jaundice appear?
A
- total bilirubin of 3-5
- this includes both direct and indirect
41
Q
Difference b/t direct and indirect bilirubin?
A
- direct bilirubin has been conjugated (water soluble) by the liver
- indirect bilirubin isn’t conjugated (not water soluble)
- if an infant with physiologic jaundice it is INDIRECT bilirubin that is high b/c liver is immature and can’t conjugate bilirubin
- In obstructive diseases - it is direct bilirubin that is elevated
42
Q
Purpose of indirect coomb’s test?
A
- tests for presence of blood type abs in serum
- pts serum is incubated with RBCs with known antigenic markers
- if there are abs present in serum they will bind to RBCs
- a positive test results in agglutination of RBCs
43
Q
What is exaggerated physiologic hyperbilirubinemia or breast feeding jaundice?
Tx?
A
- jaundice is often exagegerated when the milk takes longer to come in
- there is usually mild dehydration
- newborns should feed at a min q 2-3 hrs
- produce 6-8 wet diapers a day
- 5-6 stools a day
- Tx:
frequent feeding and adequate hydration, depending on total serum bilirubin level:
consider phototherapy (converts unconjugated bilirubin into water soluble forms that cna be excreted without conjugation in liver) - exchange transfusion if needed (rarely needed)
44
Q
Tx of jaundice?
A
phototherapy:
- use a blue light of a particular wave length with as much skin exposed as possible with eyes covered
- the light converts bilirubin to lumirubin which is excreted in the bile and urine
- risks include retinal degeneration, dehydration, hyperthermia and at times rashes
- monitor temp, hydration status, total bilirubin levels and time of exposure
Exchange transfusion:
- used when phototherapy fails or an infant shows signs of BIND, including acute bilirubin encephalopathy (reversible) and kernicterus (irreversible)
- rarely used
- irradiated blood is used to reduce risk of graft vs host disease
45
Q
RFs of phototherapy?
A
- G6PD deficiency
- sig lethargy
- temp instability
- isoimmine hemolytic disease
- albumin less than 3 g/dL
- asphyxia
- sepsis
- acidosis
46
Q
How do you diff b/t physiologic from pathologic jaundice?
A
- exaggerated physiologic jaundice occurs at serum bilirubin levels b/t 7-17 mg/dL
- levels above 17 in full term infants aren’t considered physiologic and requier further investagation
- jaundice isn’t considered physiologic if:
onset in first 24 hrs,
rate of increase of serum bilirubin exceeds 0.5 mg/dL/h - conjugated serum bilirubin exceeds 10% of total bilirubin or 2 mg/dL - obustructive problem
47
Q
increased production - causes of jaundice?
A
- hemolytic disease: ABO or Rh incompatabilities
- inherited RBC membrane defects
- G6PD
- sepsis causing hemolysis
- increased RBC breakdown:
cephalohematoma, polycythemia
48
Q
Decreased clearance - causes of jaundice?
A
- inherited liver defects, such as gilbert syndrome (liver isn’t conjugated bilirubin as effectively)
49
Q
Increased enterohepatic circulation - causes of jaundice?
A
- human milk jaundice
- breast milk jaundice
- impaired intestinal motility
50
Q
What is Caput Succedaneum?
A
- present at birth on normal vaginal delivery
- may lie on sutures, not well defined
- soft, pits on pressure
- skin ecchymotic
- size largest at birth, gradually subsides within a day
- no underlying skullbone fracture
- no tx required
51
Q
What is ceaphalhaematoma?
A
- appears within a few days after birth on normal or forceps delivery
- well defined by suture, gradually developing, hard edge
- soft, elastic but doesn’t pit on pressure
- no skin change
- become largest after birth and then disappears in 6-8 weeks to few months
- may have underlying skull fracture
- no tx reqd
52
Q
What is ABO hemolytic disease?
A
- occurs in context of mom having type O and baby having A or B
- preformed maternal anti-A or anti-B abs can passively cross placenta late in pregnancy or during delivery
- abs attack A or B ag on fetal RBCs
- about 25% of pregnancies have potential for ABO incompatibility, only around 10% of these (2.5%) develop hemolysis
- disease usually isn’t severe
- can accompany any pregnancy where mom is type O
- sxs can appear in first 24 hrs
- may develop sig anemia over first several weeks, may need to be transfused at a few weeks of age
53
Q
What is Rh hemolytic disease?
A
- much less common but more severe
- same process that occurs with ABO incompatibility but with abs directed against Rh protein
- can be more severe with each pregnancy b/c mom built up abs to Rh protein (autoimmunized)
- can accompany any pregnancy where mom has Rh - blood
- sxs in first 24 hrs
54
Q
Rh hemolytic disease (Rh isoimmunization) - how can it be prevented? What happens in severe cases?
A
usually can be prevented using Rhogam:
- immune globulin
- admin to any Rh neg woman after any invasive procedure during pregnancy as well as after any miscarriage, abortion, or delivery of Rh + infant
- impt b/c mother will never be sensitized to Rh+ antigen
- ERythroblastosis fetalis (hydrops fetalis): occurs in severe cases, especially in Rh - women who haven’t received appropriate care with Rhogam previously
- often results in fetal or neonatal death w/o appropriate prentatal intervention
- less severe cases result in hemolysis with resultant hyperbilirubinemia and anemia
55
Q
Tx of Rh hemolytic disease?
A
- when dx prenatally, transfusion of fetus with Rh (-) cells is done
- following delivery, phototherapy is started immed with exchange transfusion as necessary
- ongoing hemolysis will occur until maternal ab gone
- infants should be carefully followed for 2 months to ensure they don’t become anemic enough to warrant further transfusions
56
Q
What is human milk jaundice? Tx?
A
- prolonged unconjugated hyperbilirubinemia
- uncommon
- etiology unclear, may be assoc with b- glucuronidase, enzyme found in breast milk
- lasts 3 weeks to 3 months in thriving infant w/o evidence of hemolysis or other disease
- peaks at 10-15 days, with max bilirubin level of 10-30 mg/dL
-tx:
nursing is interrupted for 24-48 hrs
bilirubin level falls quickly and won’t rebound to same level when nursing is resumed
57
Q
What is breast milk jaundice? Rfs?
Tx?
A
- usually occurs when breastfeeding is difficult
- occurs during first week of life
- lactation difficulties lead to inadequate intake with wt loss and fluid loss leading to dehydration
- this results in slower bilirubin excretion and increased enterohepatic circulation
- RFs:
- inadequate education from clinicians and lactation consults
- inadeq documentaion of latching on by infant
- inadeq recording of urine putput and stool pattern changes
- mother and infant breast feeding complications***
- short hospital stays
- first time mothers
- Tx: education!!!! supplemenetal feeding with pumped breast milk or formula for adequate hydration and reversal of hypovolemia if necessary
- phototherapy if necessary
- prevention!!
58
Q
Total serum bilirubin estimation with degree of caudal extension?
A
- face: 5 mg/dL
- upper chest: 10 mg/dL
- abdomen: 12 mg/dL
- palms and soles: greater than 15 mg/dL
59
Q
When should you suspect pathologic cause of jaundice?
A
- if jaundice is seen in first 24 hrs (usually caused by hemolysis - medical emergency)
- TB is greater than 95th percentile
- rate of TB rise is greater than 0.2 mg/dL per hour
- jaundice in newborn greater than 2 weeks of age
- direct bilirubin greater than 1 mg/dL if TB is less than 5 mg/dL or more than 20% of TB is direct with TB greater than 5 mg/dL (suggests cholestasis)
60
Q
Common etiologies of unconjugated hyperbilirubinemia?
A
with hemolysis:
- blood group incompatibility: ABO, Rh, Kell, duffy
- sepsis
- polycythemia
w/o hemolysis:
- physiologic jaundice
- human milk jaundice
- breast milk jaundice
- internal hemorrhage (cephalohematoma)
- infant of diabetic mother
61
Q
What is SIDS? RFs?
A
- unexplained death under 1 yo
- peaks b/t 2-4 months
- most occur in infants aged a few weeks to 6 months
- RFs:
sleeping position - belly
bottle feeding
maternal smoking (pre and postnatal)
infant overheating - modifying risk factors:
back to sleep and eliminate smoke exposure
