Selected Obstetric complications - infant / maternal Flashcards
Selected Obstetric complications - infant examples ?
Meconium aspiration
Gastroschisis
Respiratory Distress
Syndrome
Necrotizing Enterocolitis
Retinopathy of Prematurity
Polycythemia
Hyperbilirubinemia
Conjunctivitis
meconium ?
Meconium-stained amniotic fluid in 10-20% of deliveries
Passage in utero often means fetal distress
If active and crying, no intervention needed
If distress, intubate and suction before stimulating to avoid aspiration
gastroschisis patho ?
Herniation of abdominal contents through an abdominal wall defect. Intestines are unprotected by peritoneum
gastroschisis: Omphalocele ?
defect is the umbilical portion and there IS a peritoneal sac covering the herniated contents
less bad cause still peritineum coverage
Both require emergent care and surgery
Respiratory distress syndrome (RDS) causes ?
Premature infants and with diabetic mothers
Respiratory distress syndrome (RDS) aka ?
Formerly known as hyaline membrane disease
Respiratory distress syndrome (RDS) patho ?
Deficient in surfactant which reduces surface tension in alveoli. ↓ amounts result in microatelectasis, “ground glass” on CXR
Respiratory distress syndrome (RDS) Tx. ?
Give corticosteroids to mothers at risk for delivery before 32-34 weeks to help lung maturation
Some may need supplemental O2 or CPAP, too
Preterm babies get prophylactic surfactant before 15 mins of age with extra doses prn
Respiratory distress syndrome (RDS) risks ?
chronic lung disease
RDS limit what ?
Limit O2 to avoid HYPERoxia. Keep O2 sats in 80’s or low 90’s for premies
Necrotizing enterocolitis (NEC) mostly seen in ?
premies
10% of cases in term babies
Necrotizing enterocolitis (NEC) etiology ?
UKN
Necrotizing enterocolitis (NEC) occurs less in ?
breastfed babies
Necrotizing enterocolitis (NEC) presentation / S & S ?
Variable presentation
Abdominal distention, emesis, bloody stools or
Apnea, temp fluctuation, lethargy
Necrotizing enterocolitis (NEC) hallmark ?
intestinal pneumatosis on abd x-ray
bacteria in bowel wall producing hydrogen
Necrotizing enterocolitis (NEC) Tx. ?
Antibiotics 10-14 days, no P.O. feeds
Necrotizing enterocolitis (NEC) prognosis ?
Free air = perf = surgery
75% survive, but many complications
Retinopathy of prematurity (ROP) seen in ?
premies
Retinopathy of prematurity (ROP) patho ?
unclear, but vessel development stops, then proliferates, especially in HYPERoxia
Retinopathy of prematurity (ROP) prognosis ?
80-90% spontaneously resolve
Rare – retinal detachment
Retinopathy of prematurity (ROP) Tx. ?
Serial exams to watch for need for surgery
Second most common cause of blindness in children ?
ROP
Retina usually vascularized by ?
36-40 weeks
Early delivery = avascular regions
Polycythemia is when HcT is at ?
When central venous Hct is >65%
Polycythemia Etiology ?
↑ in utero erythropoiesis, usually 2⁰ to placental insufficiency
Maternofetal or twin-twin transfusion
Polycythemia patho ?
↑ blood viscosity
Can cause CHF from volume overload
polycythemia problems ?
Impaired blood flow, ↓ oxygen supply
Risk of thrombotic stroke
polycythemia Tx. ?
If >70%, partial exchange transfusion with isotonic saline to ↓ viscosity
IV hydration if Hct not too severe and not symptomatic
polycythemia goal ?
55% Hct
hyperbilirubinemia prevalence ?
Common – 60-70% of infants have elevated levels
hyperbilirubinemia most cases are ?
benign and resolve
hyperbilirubinemia patho ?
Severe elevations of unconjugated bilirubin can cause neurologic damage (kernicterus)
hyperbilirubinemia physiology ?
Hemoglobin breaks down, producing unconjugated bili. This is fat-soluble, but not water-soluble, so it can cross the blood-brain barrier, but cannot be excreted.
When bili is carried to the liver, it is conjugated to a water-soluble form
But infant’s liver is immature, plus RBC life-span is shorter, plus increased red cell mass, so elevated levels of bilirubin
hyperbilirubinemia causes: Increased hemolysis
?
G6PD deficiency
Morphology changes
Rh incompatibility
Sepsis
hyperbilirubinemia causes: Decreased rate of conjugation ?
Inborn errors of metabolism
Enzyme defects
hyperbilirubinemia causes: Impeded excretion ?
Obstructed biliary flow
GI obstruction
Hyperbilirubinemia PE ?
Infants are jaundiced
**early jaundice if the first day of life is bad but 3rd day of like it is NL no so concerning **
Hyperbilirubinemia: Check total serum bilirubin ?
conjugated or not
Hyperbilirubinemia: conjugated ?
Check for biliary obstruction or hepatocellular damage or sepsis
Hyperbilirubinemia: unconjugated ?
Phototherapy will cause conjugation to a water-soluble form that can be excreted
Hyperbilirubinemia: Tx: Phototherapy ?
Causes conjugation
Bili can be excreted by
kidneys and GI tract
Liberal IV fluids needed
If infant is well, continue oral feedings
phototherapy ?only helps with unconjugated bilirubin
Hyperbilirubinemia: Tx: exchange transfusion ?
When TSB continues to rise despite phototherapy
Hyperbilirubinemia summary ?
Early elevations in bili –worrisome
Continued or late elevations – often physiologic
conjunctivitis information - whole slide ?
Standard care for newborns to receive erythromycin 0.5% ointment immediately after delivery
If discharge is noted (along with erythema, which differentiates it from nasolacrimal duct obstruction), get a culture
Chlamydia and gonorrhea – notable causes
Gonorrhea can lead to blindness
Chlamydia can be associated with pneumonia
Selected Obstetric complications - mother examples ?
Amniotic Fluid Embolism
Disseminated Intravascular Coagulation
Also, shock, PE, ARDS, MI, etc.
Amniotic fluid embolism prevalence ?
Rare complication of delivery
Amniotic fluid embolism: Normally only _____ of amniotic fluid goes into the maternal circulation during labor
1-2 mL
Amniotic fluid embolism: For an ________ to occur, more fluid must transfer (into lacerated cervical or uterine veins, placental implantation site, etc.)
embolism
Amniotic fluid embolism: what, possibly meconium into maternal bloodstream
Fetal debris, lanugo, vernix
Amniotic fluid embolism aka ?
“Anaphylactoid syndrome of pregnancy”
Amniotic fluid embolism S&S ?
Sudden resp distress, CV collapse, coagulopathy
Amniotic fluid embolism prevention ?
Unpreventable
Amniotic fluid embolism Tx. ?
supportive, maintain O2 and BP and manage coagulopathies
Amniotic fluid embolism prognosis ?
Mortality rates 26-80%
25% die within first hour
80% die within first 9 hours
Disseminated intravascular coagulation (DIC) patho ?
Inappropriate activation of coagulation and fibrinolytic systems
Disseminated intravascular coagulation (DIC) secondary to another event such as ?
Placenta abruption (most common obstetric cause)
Placenta previa
Pre-eclampsia, eclampsia
Retained dead fetus
HELLP syndrome
Amniotic fluid embolism
Disseminated intravascular coagulation (DIC) physiology ?
Pregnancy and puerperium are already hypercoagulable states with increased activity of coagulation factors
Event occurs, triggering cascade of clotting factors
Small thrombi form in the blood vessels and cut off blood supply to various organs such as the liver, brain, or kidney. These organs will then be damaged and may stop functioning.
Over time, the clotting proteins are consumed or “used up“ and patient is then at risk for serious bleeding, even from a minor injury or without injury. This process may also break up healthy red blood cells.
Disseminated intravascular coagulation (DIC) S&S ?
generalized bleeding,
purpura,
petechiae,
fever,
proteinuria,
hypotension
Disseminated intravascular coagulation (DIC) Tx. ?
In most cases, termination of the pregnancy
Supportive therapy
Disseminated intravascular coagulation (DIC) prognosis ?
Guided more by the cause than the coagulopathy
Most moms will improve with delivery or evacuation of the uterus
