Transition out of the Perinatal Period Flashcards
Perinatal catecholamine surge
At birth, there is a massige surge in epinephrine and norepinephrine in the infant, which lasts for approximately four hours
This facilitates the increased cardiac output and myocardial contractility, increased pulmonary surfactant production, and promotes reabsorption of fluid in the lungs. Heart rate is usually ~160 bpm and drops to ~130 bpm 1 hour after birth.
It also enhances gluconeogenesis and lipolysis, mobilizing fuel for breathing and feeding.
Changing flow through the ductus arteriosus after birth
As pulmonary vascular resistance declines, the right-to-left shunt through the ductus arteriosus becomes bidirectional, then left-to-right.
A combination of increased oxygenation and diminished signaling from placental PGE2 are responsible for the ductus’ closure in the weeks following birth.
The ductus is at risk of premature closure if NSAIDs are used after 33 weeks EGA, as it will shut down placental PGE2 production.
Misoprostol vs dinoprostone vs dinoprost
Misoprostol: PGE1
Dinoprostone: PGE2
Dinoprost: PGF2a
Respiratory syndromes that may prevent proper cardiovascular transition in neonates
- Meconium aspiration
- Amniotic fluid aspiration
- Respiratory distress syndrome of the newborn (surfactant deficiency)
- Pneumonia or other lung infections
- Congenital hypoplastic lungs (as in diaphragmatic hernia or oligohydramnios)
Premature closure of the ductus arteriosus leads to a syndrome of. . .
. . . pulmonary hypertension with cyanosis and respiratory distress
This usually presents shortly after birth in a case where the mother has used NSAIDs during the third trimester (after EGA 33)
Transient tachypnea of the newborn
- Onset at birth, mild course, lasts 48-72 hours and resolves spontaneously
- Baby will be tachypneic and grunting (to raise EEP)
- Diagnose with CXR (shows hyperextended, wet lungs)
- Treat w/ positive pressure ventilation
- Thought to be due to delayed reabsorption of pulmonary fluid and consequentially low pulmonary compliance. Mechanistically, low catecholamine surge at birth has been implicated.
- Risk factors: Cesarean section, Excess maternal analgesia, birth asphyxia, excessive maternal fluid administration, breech delivery, delayed cord clamping, fetal polycythemia
While functional ductus arteriosus closure occurs in virtually 100% of infants by ___, permanent anatomic ductus arteriosus closure may occur ____.
While functional ductus arteriosus closure occurs in virtually 100% of infants by 4 days, permanent anatomic ductus arteriosus closure may occur months later or not at all.
Transitional cardiac abnormalities in infants from GDM pregnancies
Presumably due to the cardiac growth-stimulating effects of insulin
- Asymptomatic cardiomyopathy
- Hypertrophic subaortic stenosis
Transitional cardiac abnormalities in infants born to mothers with anti-Ro or Anti-La
5% risk of congenital heart block due to deposition of transplacentally acquired antibody
Neonatal Grave’s disease
- Heart failure
- Goiter
- Tachycardia
- Low weight
- Failure to thrive
- Proptosis
Ritodrine neonatal cardiac effects
Associated with neonatal interventricular septal hypertrophy
Respiratory rate in healthy newborns
Newborns are typically born with tachypnea which stays relatively constant for 6 hours, then regresses to what we expect for an infant.
Apnea of the neonate (differential)
- Sepsis
- Intracranial hemorrhage
- Hypocalcemia
- Hypoglycemia
- Seizure
- Maternal myasthenia gravis
- Maternal drugs (especially narcotics, benzodiazepines, magnesium sulfate)
Pulse oximetry in a newborn
Usually does not reach 90% until ~9 minutes after birth
Neonatal dependence upon gluconeogenesis and glycogenolysis
During the first few days, only ~20-50% of the glucose utilized for energy comes from milk. All the rest is produced by hepatic metabolism.
Fat metabolism and ketone metabolism are also highly active during this time as suppleental energy sources.
Etiologies of transient neonatal hypoglycemia
- Fetal: IUGR (low glycogen stores), LGA (unknown etiology), erythroblastosis fetalis-associated hyperinsulinemia, infection, hyperviscosity syndrome
- Maternal: GDM, excessive intrapartum parenteral glucose administration, beta-sympathomimetic tocolytics, oral hypoglycemics
Symptoms of neonatal hypoglycemia
- Jiteriness
- Irritability
- Lethargy
- Cyanosis
- Apnea
- Seizures
- Poor feeding
- Unexplained respiratory distress
- Abnormal cry
Defining hypoglycemia in neonates
Neonates have much lower physiologic blood sugars than children or adults, with sugars of ~35mg/dL being relatively normal.
That said, most clinicians would define neonatal hypoglycemia as plasma sugar < 40 mg/dL with symptoms at any postnatal age
Fetal calcium regulation
In the fetus, PTH and calcitriol are low, but calcitonin is high, favoring calcum deposition into bones.
Shift in calcium homeostasis in the neonate
During the fetal period, calcitonin is the predominant hormone and PTH levels are very low.
Following delivery, calcium levels begin to drop over time, stimulating PTH and calcitriol. This begins bone resorption, sensitizes the gut to absorb calcium, and causes reabsorption of calcium at the nephron.
Calcium levels stabilize around 8 mg/dL by 48 hours and gradually rise to reference range over the next several weeks.
Neonatal hypocalcemia
May be asymptomatic or may present similarly to hypoglycemia (jitteriness, poor feeding, seizures, cyanosis) along with increased tone.
Usually between 24-48 hours age.
Natal transfusion
At the time of birth, the placenta delivers an effective transfusion to the infant due to contraction of the uterine wall.
This is an important determinant of blood and plasma volume within the first few postnatal days.
This amounts to a rise of about 1-2g/dL Hgb
Effects of delaying cord clamping by 3 minutes and holding the baby below the level of the introitus
These would increase the amount of blood transfused from the placenta into the neonate, potentially by up to 50%.
This may result in polycythemia and subsequent hyperbilirubinemia
Etiologies of neonatal polycythemia
- Excessive placental transfusion
- Twin-twin transfusion syndrome
- Gestational diabetes mellitus
- Fetal hypoxia (may be due to placental insufficiency, toxemia, postmaturity syndrome, maternal smoking)
- Thyrotoxicosis
- Congenital adrenal hyperplasia
- Down syndrome
Definition of polycythemia in a newborn
Venous hematocrit > 65%
Symptoms of polycythemia in the newborn
- Plethora
- Irritability
- Poor feeding
- Seizures
- Apnea
- Abnormal cry
- Respiratory distress
- Hypoglycemia
- Necotizing enterocolitis
- Oliguria with hematuria
Definition of neonatal anemia
Hematocrit of <42% immediately after birth
Whether delayed cord clamping transfuses the infant, or drains blood from the infant, depends entirely upon. . .
. . . gravity
Manifestations of hemorrhagic disease of the newborn in infants who do not receive a vitamin K bolus
Manifests 1-7 days following delivery with bleeding from cutaneous, gastrointestinal, or circumcisional sites.
Generally speaking, the GI tract of the neonate is characterized by ___ in the first few days
Generally speaking, the GI tract of the neonate is characterized by discoordination and hypomotility in the first few days
Possibly due to maternal progesterone, same as for mom. The esophagus is more discoordinated than hypomotile, but stomach emptying is delayed and the esophageal sphincter is tonically relaxed.
First feeding
The first feeding of the newborn, parallel to its first breath, stimulates the GI system through the release of GI-active hormones: gastrin, enteroglucagon, and motilin.
This “wakes the gut up”, as it were, and increases the baby’s GI motility – paricularly below the diaphragm.
___ is found to be prematurely elevated in infants that pass meconium in utero.
Motilin is found to be prematurely elevated in infants that pass meconium in utero.
Meconium plug syndrome
- Presents as delayed stool passage with signs of obstruction
- Observed disproportionately in GDM
- Hypothesized that fetal hypoglycemia-induced hyperglucagonemia leads to poor gut motility in the neonate
Birth trauma and oligo/anuria
Birth trauma that is significant enough to induce neonatal rhabdomyolysis may lead to renal failure in the newborn
Maternal drugs that may damage the fetal kidneys
- ACE inhibitors
- ARBs
- Aminoglycosides
- Amphotericin B
- Acyclovir
- Indomethacin
- Radioactive contrast
Manifestations of neonatal intracranial hemorrhage
- Apnea
- Seizures
- Neurologic deficits
Anemia and polycythemia of the newborn usually present. . .
. . . from birth
Hemorrhagic disease associated with maternal drugs usually presents. . .
. . . on postnatal day 1
Transient hypoglycemia of the neonate occurs ___, while transient hypocalcemia of the neonate occurs ___.
Transient hypoglycemia of the neonate occurs 1-2 hours after delivery, while transient hypocalcemia of the neonate occurs 24-48 hours after delivery.
These are both very uncommon in infants without risk factors
___ usually present without risk factors, but passage of stool on the first day make these diagnoses unlikely.
Meconium plug syndrome and small left colon syndrome usually present without risk factors, but passage of stool on the first day make these diagnoses unlikely.
Small left colon syndrome
- Dysfunctional, diminutive left colon that causes transient obstructive symptoms
- ~50% of cases associated with GDMA2 (insulin-dependent)
- Manifests in first 24-48 hours of life
- If detected early, can be cured by radiographic contrast enemas
Radiographic contrast enema is both diagnostic and therapeutic for. . .
. . . BOTH small left colon syndrome AND meconium plug syndrome
Progression of a newborn’s SpO2
At birth, ~60-65% is normal
Should reach 90% after about 10 minutes
Treating primary apnea
-
First line: Stimulation!!!
- Rub back w/ towels
- Tapping feet
-
Second line: Suctioning (done for many infants anyway)
- To prevent meconium aspiration
- Third line: Positive pressure ventilation
- Fourth line: Intubation
If a newborn has neonatal bradycardia (HR < 100), the first-line therapy is. . .
. . . positive pressure ventilation
Neonatal primary bradycardia is likely due to an oxygenation problem. Once oxygenation is fixed, then you can re-assess.
But, if this fails to help or if baby has signs of good ventilation (good chest movement, respiratory rate, decent oxygen saturation within the 80’s), then you begin 3:1 CPR and umbilical vein epinephrine.
If baby is breathing, but oxygen saturation is still poor, what is the treatment?
First line: FiO2 increase (supplemental oxygen)
Second line: Positive pressure ventilation
Third line: Intubation
What defines a “1” in the various APGAR categories? (since 0 and 2 are obvious)
- Appearance: Acrocyanosis
- Pulse: Palpable, but <100 bpm
- Grimace: Present only after excessive stimulation
- Activity: Flexion, but no resistance to extension – basically weak for a baby
- Respirations: Irregular
CXR in transient tachypnea of the newborn vs respiratory distress syndrome of the newborn
TTN: Hyperextended lungs w/ fluid
RDS: Hypoextended lungs w/ prominent atelectasis
Treatment of RDS of the newborn
Intubation +/- surfactant administration
An infant should pass meconium by ___ following delivery
An infant should pass meconium by 48 hours following delivery
Otherwise, the diagnosis is failure to pass meconium (FTPM), which may indicate some GI obstruction or motility.
Major etiologies of failure to pass meconium
- Imperforate anus
- Meconium ileus
- Hirschprung’s disease
What is the one thing you should NEVER do to an infant with imperforate anus?
Try to take a rectal temperature
When you do this, you are effectively stabbing into the peritoneum. This may cause peritonitis and serious infection.
Diagnosis and treatment of imperforate anus
- Diagnosis: Cross-table X-ray
- Treament:
- Before anything else: Most of these patients will have VACTERL syndrome. So, before doing anything else, do an ultrasound of sacrum, echocardiogram, and endotrachealcatheter with X-ray, voiding cystourethrogram, and X-ray of wrists. The tracheoesophageal fistula in particular may limit your ability to do surgery, and so this needs to be addressed before fixing the imperforate anus.
- Mild: ie, when the imperforate anus is where it should be and only a small septum is in-between. Can be surgically corrected immediately after birth.
- Severe: ie, anal canal is nowhere near where it should be to connect to the perineum. Do a colostomy now, then fix at a later date once baby can better tolerate a more invasive surgery.
Meconium ileus
- Most cases will be due to cystic fibrosis
- Effectively the pathology is that of CF: Not enough fluid is pumped into the GI lumen, and so the bolus is sticky and non-motile, causing bowel obstruction.
- Presents as failure to pass meconium, often in someone who has had no prenatal care or is known to be at risk for CF.
- Diagnosis: X-ray demonstrating transition point, sometimes with gass-filled plug.
- Treatment:
- For the ileus: Water enema or water-contrast enema (aka gastrographin)
- For likely CF: Sweat chloride test, supplement fat soluble vitamins and pancreatic enzymes, install pulmonary toilet.
Hirschprung’s disease
- Caused by a failure of distal migration of inhibitory neurons in Auerbach’s and Meissner’s plexi. Since the migration always occurs proximal to distal, the distrubition of the disease is a lot like UC – a continuous band from the distal-most colon to a more proximal point.
- The rectal sphincter cannot relax since there is no inhibitory neuron to interrupt its tone.
- Most present w/ failure to pass meconium, palpable colon, and explosive diarrhea on digital rectal exam in an infant. Some will present with chronic diarrhea and overflow incontinence later in childhood.
- Diagnosis: X-ray showing a portion of distal, non-dilated colon (a dilated colon would be a good sign!). For FTPM, gastrographin enema is the next step. For later childhood presentations, ano-rectal manometry is the next step. The diagnosis in both cases is confirmed by biopsy showing absence of these plexi.
- Treatment: Surgical resection of “bad” colon.
When should you be concerned vs not concerned about baby emesis?
Not concerned: Non-projectile, non-bilious, formula-colored emesis following eating
Concerned: Projectile bilious or non-bilious emesis.
Bilious emesis is ___
Bilious emesis is green
Malrotation syndrome
- Pathogenesis: Failure of gut to rotate as it re-enters the abdomen in embryologic development. One loop of bowel strangulates another.
- Presentation: Normal, uncomplicated prenatal course. Baby displays projectile bilious emesis.
- Diagnosis: X-ray showing double-bubble, but normal gas pattern beyond. Confirm with upper GI series.
- Treatment:
- Conservative: NG tube with intermittent suction to decrompress
- Definitive therapy as followup: Surgery to correct volvulus
Duodenal atersia
- Failure of re-canulization of the duodenum resulting in complete small bowel obstruction.
- Presentation: Polyhydramnios in prenatal course. Associated w/ Down syndrome. Baby presents with projectile biliary emesis.
- Diagnosis: X-ray showing double bubble WITHOUT air beyond.
- Treatment: Surgery.
Annular Pancreas
- Strangulation of a segment of duodenum by the pancreas. Ultimately due to failure of apoptosis of embryologic pancreatic structures.
- Presentation: Polyhydramnios in prenatal course. Associated with Down’s syndrome.
- Diagnosis: Double bubble sign WITHOUT gas beyond obstruction.
- Treatment: Surgery.
Annular Pancreas and Duodenal atresia. . .
. . . look exactly the same
Same risk factors, same prenatal course, same presentation, and same diagnostic imaging.
You only know which is which when you go in for therapeutic surgery.
Intestinal atresia
- Caused by vascular accidents in utero (vasospasm cuts off blood supply to developing gut).
- Presentation: Mom uses some vasoconstrictive agent (often cocaine) or has an arterial thrombotic disease (like APLS). Polyhydramnios may or may not be present. Not associated with Down’s.
- Diagnosis: X-ray showing double-bubble AND multiple air-fluid levels (ie, multiple segments of atresia)
- Treatment: Surgery
- May precipitate short-gut syndrome and consequent malabsorption
Tracheoesopageal fistula
- Presents as non-biliary emesis with prominent gurgling and bubbling (since baby is breathing through gastric secretions), usually on the first day of life
- Diagnosis: NG tube that coils on X-ray (Board favorite quesiton to ask)
- Treatment: Parenteral nutrition as bridge to surgery
- Followup with workup for VACTERL
Pyloric stenosis
- Hypertrophy of the pylorus leading to gastric outlet obstruction. Typically occurs at week 2-8 of life after a history of normal feeding.
- Presentation: Projectile, non-bilious vomiting. More common in males.
- Buzz-words: Olive-shaped mass, visible peristaltic waves on exam
- Diagnosis: CHEM20 showing hypochloremic, hypokalemic metabolic alkalosis. Ultrasound showing a “donut sign”
- Treatment: IV fluids to correct chloride-deficient metabolic alkalosis. Pyloromyotomy.
- NOTE: This is a Boards favorite. You workup and treat the metabolic alkalosis BEFORE doing your ultrasound and going to surgery. Treat the metabolic disturbance FIRST, THEN the underlying pathology.
Brief resolved unexplained event (BRUE)
- Change in color, tone, breathing, or responsiveness
- Patient must be < 1 y.o. and event must last < 1 minute
-
Low risk:
- Absence of cyanosis, murmur, fever, signs of abuse
- First time event
- Term baby > 60 days old
- Do nothing. Reassure parents.
-
High risk:
- Presence of cyanosis, murmur, fever, or signs of abuse
- Repeat event
- Premature < 32 weeks or post-term > 45 weeks
- History-guided laboratory studies
SIDS
- Child that dies for no explainable reason, not even on autopsy
- Only diagnosed retroactively AFTER autopsy is inconclusive
- Premature infants and infants with congenital defects are at higher risk
-
Prevention:
- Lay infant on their back when in cradle
- Do not share a bed with the baby, ever
- Smoking cessation
- There is no effective screening for SIDS, even for those at high risk.
Physiologic anemia in a neonate
- Between 3-9 months of age
- Effects of oxygenation on HIF1a expression and EPO -> takes time!
- Premature cord clamping
- Hemolysis of any etiology (most commonly a benign ABO hemolysis of newborns)
- Iron deficiency, even to a small degree, is also common!
Indications for bag-and-mask PPV at birth
- HR < 100 bpm
- Gasping respiratory effort
- Apnea
Management of clavicular fracture in a newborn (without gross deformity)
Pin their sleeve to their shirt
After 2 weeks, proper healing should be confirmed either via clinical findings of a callus formation, and possibly an x-ray. The condition usually self-resolves within 2–3 weeks without surgical intervention or long-term complications.
While technically strawberry hemangiomas can be treated with topical beta blockers (timolol) or corticosteroids if desired by parents, the right answer on the test is. . .
. . . do nothing
