Complications in Newborns: Day 1

Name 2 reasons for RDS or respiratory distress syndrome. What percent chance do babies have of getting if they are born prior to 28 weeks gestation?

1. lack of surfactant

2. immature development of lungs

50% chance of developing in babies born prior to 28 weeks.

Name some RDS acute complications:

1. pneumothorax: due to invasive mechanical ventilation

2. Infection: due to multiple invasive procedures

3. Intraventricular hemorrhage (in the brain): due to unstable hemodynamics

Name some RDS long-term complications:

1. Bronchopulmonary dysplasia: due to inflammation and prolonged damage to the delicate lung tissue during mechanical ventilation.

2. Retinopathy of prematurity: due to high concentrations of supplemental O2 hearing and visual disability, cerebral palsy and learning and developmental delays.

What is intraventricular hemorrhage

Bleeding inside or around the ventricles in the brain that contain the cerebrospinal fluid.​

What is patent ductus arteriosus (PDA)

A persistent opening between the aorta and pulmonary arteries leading from the heart.​

What is bronchopulmonary dysplasia

A chronic lung disease caused by high volume or pressure from mechanical ventilation that damages lung tissues. Incidence increases with decreasing gestational age of a premature newborn.​

What is retinopathy of prematurity

Disease involving the vessels of the retina, which may lead to vision loss or blindness.​

Name 4 ways to prevent/address RDS(respiratory distress syndrome).

1. prevent preterm birth

2. Antenatal corticosteroids (23 to 34 weeks) = matures lungs, increases surfactant (this is on the test. When moms go into premature labor, we give them corticosteroids to help baby’s lungs mature and increase surfactant).

3. Post-birth surfactant therapy

4. NPO advance feeding (increased tube feedings)

What are the 3 distinguishers of apnea of prematurity

1. cessation of breathing for >20 seconds or

2. cessation of breathing <20 but with bradycardia(<80/min) or

3. cessation of breathing <20 seconds with an O2 saturation of <85%

Name a few reasons why/how apnea of prematurity occurs. Name a few minfestations.

This occurs due to:

• poor neuromuscular control

• instability of the upper airway

• immature breathing control center in the brain

Clinical Manifestations​

 Pallor​

 Dusky skin tone​

 Cyanosis​

 Comorbidities​

 Obstructed breathing​

 Infection​

 Metabolic Imbalances​

 Hypothermia​

 Hyperventilation​

TTN - transient tachypnea - Name a few manifestations. Name a few interventions.

What are some manifestations?

• rapid/shallow respiratory effort

• tachypnea

• nasal flaring

• intercostal/subcostal/substernal retractions

• tachycardia

• cyanosis

What are some interventions.

• respiratory support - provide cannulas, CPAP, oxyhood, etc.

• thermoregulation management

• nutritional therapy - provide parenteral nutritional support (IV) to prevent hypoglycemia and do at 60 - 80 mL/kg/day if respirator rate is over 80/min to avoid aspiration risk. Cannot do oral feedings until TTN resolves.

• continuous non-invasive pulse oximetry and assess ductal shunting (are the ducts still open in the heart which is why they are struggling for O2?)

• respiratory and cardiac monitoring - measure arterial blood gasses frequently for hypercapnia (increased O2).

• chest x-ray

• CBC with diff, blood cultures, CRP, lactate levels

• broad spectrum antibiotics for 24-48 hours until sepsis is ruled out.

• anticipate NICU admission after post-resuscitation

How does meconium aspiration syndrome occur? Comorbidities? What populations is it a higher chance in? Manifestations?

How does it occur?

1. Uterine stress results in the newborn having a BM (meconium) in utero

2. Other risk factors: fetal distress, cesarean birth, maternal diabetes and HTN, being term or post-mature and difficult birth.

3. gasping reflex of the newborn at birth results in the infant drawing in the meconium-stained fluid into its lungs.

Comorbidities?

• Infection

• TTN transient tachypnea of newborn

• pulmonary HTN

• Right-to-left shunting through patent ductus arteriosus

Populations:

• black babies

• term or post-term babies

Manifestations:

• mild to severe respiratory distress

• tachypnea, grunting, nasal flaring, bradycardia, hypoxemia, apnea, and cyanosis.

• being limp or floppy

• Coarse crackles upon lung auscultation

• Meconium-stained skin, nails or umbilical cord

What is esophageal atresia (EA) and tracheoesophageal fistula (TEF)?

EA: abnormality where the esophagus doesn’t form a continuous passage into the stomach. Prevents newborn from swallowing amniotic fluid due to incomplete esophagus.

TEF: often associated with TEF which is an abnormal connection between the esophagus and trachea. This may occur at many points and many ways.

Both can cause aspiration due to secretions going into the lungs.

What is proximal TEF and distal TEF (there are others but focus on these)?

Proximal TEF: connection that enables saliva secretions to flow down and enter the lungs.

Distal TEF: stomach contents can reflux into the lungs.

What is polyhydramnios?

Polyhydramnios: excess fluid around the fetus. This is due to fetal EA which prevents the baby from swallowing amniotic fluid.

Associated syndromes:

1. VACTERL syndrome: congenital abnormalities like vertebral and cardiac defects

2. CHARGE syndrome: heart defects, genital abnormalities.

How does EA occur in development and how does this, mixed with polyhydramnios impact the fetus?

EA develops due to the foregut failing to properly separate or just being underdeveloped.

EA&Polyhydramnios impact on the fetus?

• premature labor due to overdistended uterus

• prematurity or SGA

• newborn cannot handle normal amounts of fluid and saliva increaing the risk of aspiration pneumonia

• crying, straining or ventilation may lead to gastric perforation(hole in stomach)

EA and TEF management:

• immediate stabilization of respiratory system to ensure patent airway, maximize ventilation and prevent aspiration

• stabilization during feeding

• Fowler’s position or high fowlers to reduce aspiration

• Oral care and suctioning

What is a brachial plexus injury and the other name for it? What things can cause this? What parts does it impact on the body? What are some manifestations of erbs palsy?

This is a peripheral nervous system injury and can also be called Duchenne-erb (Erb’s) palsy. It is caused by a stretched brachial plexus.

This can be caused by large birth weight, shoulder dystocia(shoulder stuck in birth), or breech birth.

This can impact shoulder, arm or hand function. Can also occur with skeletal trauma like clavicle or humerus fractures.

Manifestations: limited shoulder movement, elbow extension and positioning of the affected arm. Reflexes like moro, biceps and radial are absent.

What is facial nerve palsy and manifestations?

Definition: Damage of facial nerves resulting from compression of fetal head from birth or forceps.

Manifestations: asymmetry of the face during crying, drooping corner of the mouth, smooth swollen face on the affected side.

What is omphalocele? What is gastroschisis? What is the difference? This will be on the test.

Omphalocele: covered defect in the umbilical ring. Common with preterm. There is an underlying chromosomal defect (12, 18, 21). The sac may rupture during birth. We do not want it to. Cover with a sterile, non-adherent dressing to help it go down if it didn’t rupture.

Gastroschisis: herniation of bowels though a defect in the abdominal wall. It occurs right of the umbilical ring. There is no covering membrane. This is 3-4x more likely. It is a big infection risk.

What is a shunt?

A tube for drainage

Explain the difference between anacephaly, encephalocele and microcephaly. What causes both anacephaly and encephalocele? What causes microcephaly and what can you do to prevent it?

Anacephaly and encephalocele are both caused by failure of anterior end of neural tube to close.

Anacephaly: absence of both cerebral hemispheres. Incompatible with life.

Encephalocele: Herneation of brain and meninges through skull defect. Needs surgical repair and shunt to prevent hydrocephalis. High risk for cognitive defect.

Microcephaly: Baby born with small head size. It can be caused if the mom gets ZIKA virus.

• Prevent: safe sex, test early in pregnancy, vaccinate, insect repellent, mosquito nets, avoid high risk areas. ZIKA is a member of the TORCH infections (infections that can spread from mom to baby).

What is hypospadias? What maternal factors may cause this?

A urethral opening on a male baby lower on the penis. Baby may also have bladder or other GI issues.

Maternal factors:

• pregnancy over the age of 35

• maternal obesity

• exposure to estrogen in utero

Epispadias definition for males and females:

Definition:

Men: urethral opening on the dorsal(top) side of the penis. May also have a broad, short penis. The pelvic bone structure may also be widely separated.

Women: clitoral hood appears divided into 2 halves. May be urine leakage and stress incontinence.

What ways can a congenital diaphragmatic hernia be treated and monitored(many)?

1. a rapid assessment: can be diagnosed with an X-ray or ultrasound.

2. Resuscitation: avoid bag and mask ventilation. Opt for endotracheal intubation and mechanical ventilation. Umbilical arterial and venous catheters can also be inserted for fluid resuscitation and cardiovascular support.

3. Gastric tube insertion with continuous suction to prevent bowel distention and further compression of the lungs which can worsen respiratory distress.

4. Monitor pulse ox, respiratory, BP and cardiac.

5. Frequent testing for arterial blood gasses, electrolytes, ionized calcium, complete blood count, glucose and lactic acid testing.

6. Thermal regulation: newborn is placed on a radiant warmer or isolette to maintain temp

7. Chromosome testing once stabilized to identify associated genetic abnormalities.

8. Prepare family for long term stay in the NICU and surgery.

9. 
   

What risk factors for mom can lead to fetal neural tube defects? What should moms be consuming to prevent these? How much/different sources? By what percent can these defects be reduced if this thing is consumed? How much do levels of this increase while pregnant?

Risks: folic acid deficiency, diabetes, certain medications like valproic acid and excessive maternal heat.

Moms should consume 400 mg of folic acid every day. You can get it from citrus, flour and cereal that is supplemented with it.

Consuming folic acid can decrease defects by 40%

Levels increase to 600-800 mcg while pregnant.

What can cause hyperbilirubinemia? (pathologic jaundice) Can the causing condition be deadly? How can we treat the cause? (1)

Cause: mom would be RH- and baby would be RH+. This is called Rh incompatibility. Mom would see baby as a foreign antigen and attack baby’s red blood cells. See e-learning video for more.

Yes, this condition can be deadly.

Can be treated with an intrauterine transfusion.

Further caused by the presence of accumulated and unconjugated bilirubin and hemolyzed(broken) red blood cells under the skin.

What is physiologic jaundice? What percentage of prevalence in healthy term newborns?

Common to have jaundice after 24 hours of life to a few days.

Occurs in 66% of healthy term newborns.

Occurs in almost all preterm infants (37 weeks or earlier)

What can happen if pathologic jaundice is not treated?

It can develop into acute bilirubin encephalopathy after a few days then to kernicterus. This is chronic brain damage.

How long does a baby have to have jaundice for it to be considered pathologic.

Any case that lasts for longer than 14 days of life in a term infant

Hyperbilirubinemia continued: ABO incompatibility. How does this occur? How is it treated?

Fetal blood type would be A,B, or AB and moms would be O.

Mom has naturally occurring anti-A and anti-B antibodies which are transferred across the placenta to the fetus.

Exchange transfusion required occasionally.

What is hydrops fetalis? It is a symptom of pathologic jaundice.

severe swelling of baby

Why and when do we give Rhogam? What is the other name for it? Treatment?

Rhogam or RHo(D) is given at 28 weeks! (on the test) so mom’s antigens don’t attack baby if she is rh- and baby is rh+.

Treated with an exchange transfusion.

How can orofacial clefts impact baby?

impact feeding, speech, hearing, dental development and well-being

How can a cleft lip/palate be fixed?

Surgery, speech therapy and orthodontic treatment.

What is some education and things to keep in mind for a baby with a cleft lip/palate?

• small and frequent feedings when newborn is stable

• find the right nipple positioning

• airway patency can be helped along with some light suctioning

• newborn should be burped often and after every ½ or 1 ounce of milk

What is spina bifida? What may the newborn experience because of this?

It is a neural tube defect during development resulting in an incomplete closure of the spine that can lead to differing degrees of exposed neural tissue or meninges. This can be hidden or external with a fluid filled sac that protrudes.

The newborn may experience musculoskeletal impairment.

What are the 3 types of spina bifida? (least tot most protruding)

1. spina bifida occulta

2. Meningocele

3. Myelomeningocele

What would someone with myelemeningocele be allergic to?

Latex

How would you treat spina bifida and do right away?

Cover with a sterile dressing. The only way to confirm this diagnosis is with an ultrasound.

What puts baby at risk of developing spina bifida?

teratogens, pollution, radiation, poor nutrition, low folic acid, caffeine, alcohol, diabetes, anxiety and more.

By when is blood spot testing completed? What are 3 types of screening for inborn errors of metabolism? (IEM)

Phenylketonuria

Glactosemia

Congenital hypothyroidism

Complete within 24 hours. Can detect at least 50% of consequences to screen IEM - inborn errors of metabolism.

Key point

Erythroblastosis fetalis leads to anemia, edema, and the cytotoxic effects of unconjugated bilirubin.​

What is COOMBS test and what is it used for?

It determines if antibodies are attached to red blood cells of baby?

Key point

Neonatal exchange transfusion with type O, Rh-negative RBCs serves to treat anemia and acidosis and remove bilirubin, maternal antibodies, and fetal RBCs that are beginning to hemolyze.​

What is erythroblastosis fetalis?

Moms antibodies attack baby’s RBCs