pulmonary disorders p1 PPT (3/22)

When does RDS always occur (wks) and why, its MC cause, and what disease process it can lead to?

Respiratory distress syndrome, aka. hyaline membrane disease caused by surfactant deficiency. Occurs in 1% of pregnancies w/ significant incidence ALWAYS happening <28 weeks (possibly happening later), as baby’s lungs are not compliant enough.

If given high pressures, RDS can turn into → PID (acute emphysema) → BPD (bronchopulmonary dysplasia).

What does prematurity lead to (2)? What do those 2 then lead to (2)?

1. Prematurity leads to either:

   1. structurally immature lung (low FRC, high resistance, poor compliance)

   2. surfactant deficiency

      1. These 2 lead to atelectasis → VQ mismatch (bc of immature vasculature + lungs) + hypoventilation (high CO2) → hypovolemia + hypercarbia

In the RDS tree, how do acute issues progress after hypovolemia + hypercarbia?

48-72h, end of honeymoon phase:

acidosis (organs premature + don’t know how to hold bicarb) → pulmonary vasoconstriction (cord clamp should lower resistance, but patent shunts can increase it) → impaired endo/epithelial integrity → proteinaceous exudate → RDS

In the RDS tree, what O2 therapy can help chronic issues after they become hypovolemic and hypercarbic? What 2 pathways do they then lead to?

from hyper/hypo, it leads to → high FiO2 + trauma (vent) which then leads to 2 paths:

1. inflammatory response → cytokine release

2. antioxidant reduction → free-radical reactions

   Both then lead → lung injury → chronic lung disease/BPD

RDS clinical presentation/symptoms

Presentation: shows w/I min-hours after birth, and if left untreated, will rapidly worsen.

Symptoms:

1. WoB (tachy, grunting, nasal flaring, retractions)

2. cyanosis

RDS diagnosis (what specific thing do you see on CXR? BS) + problem w/ WoB

CXR: ground glass
BS: diminished bilaterally

Can tell w/ increased WoB + O2 requirements. Problem is that energy is used to increase WoB, reducing the energy used to grow organs, leading to underdeveloped organs.

How to prevent RDS in regards to birth (4)

1. PREVENT PREMATURITY. MOST IMPORTANT!!!

2. avoid unnecessary, poorly timed C-sections

3. have antenatal + intrapartum fetal monitoring

4. give atenatal steroid therapy

RDS treatment (5)

1. thermoregulation (don’t let them be cold)

2. manage fluids (reduce metabolic demands, shunts while giving fluids/nutrition can increase risk of brain bleeds)

3. PEEP (CPAP) not PIP (vent)! (minimize lung injury)

4. Surfactant (early!)

5. Prevent hypoxemia + acidosis

What happens if you give surfactant before ventilation?

Increased pressures will harm the lung without surfactant, as compliance skyrockets and pressures decrease with surfactant.

Why choose PEEP/CPAP over PIP/vent? Why choose jet over CPAP?

prevents atelectasis + pulm. edema as PIP expands + collapses lungs; whereas, PEEP expands + holds lungs @ that spot to promote recruitment

Jet ventilator evenly distributes pressure, whereas PEEP does not and can hyperventilate an area and hypoventilate another.

Why do neonates not want 100% SpO2?

do not know how well PaO2 is

What leads to a better RDS prognosis (aka likely course of the disease)

The earlier the treatment and the more gentler the treatment, the better the outcome will be. Early surfactant, steroids and gentle O2 therapy will improve mortality + morbidity.

TTNB pathology + most common cause in regards to birth?

Transient tachypnea of newborn

Babies normally have fluid in their lungs while they are still clamped; however, once they are clamped and independent, fluid from their lungs must be cleared. If it is not cleared, TTNB happens and fetal lung liquid is reabsorbed.

MC: C-section (babies need squeeze)

Clinical presentation of TTNB (5)

1. Comfortable tachypnea (80-100bpm (normal 40-60), utilizes what SA it has to ventilate)

2. peripheral cyanosis (and can also be at lips)

3. resp. acidosis (cannot rid CO2)

4. hypoxemia

5. Diminished, crackles (can be normal too depending on severity)

How to diagnose TTNB? (2)

Only able to diagnose off exclusion (e.g., if tachypnic and other clinical signs do not add up to another disease process? TTNB.) with the aid of CXR.

What O2 devices should you use for TTNB? Why? (2)

Bubble CPAP or HFNC only w/ >60% FiO2. Only need to work fluid out!

Neonatal pneumonia ways for transmission (3)+ huge risk?

>10% of infants that got pneumonia through either intrauterine, intrapartum (ascending vertical transmission) or postnatal.

HUGE risk if mom doesn’t know she’s in labor but has GBS, as it can be passed down.

Types of neonatal pneumonia's (3) for late and early? Antibiotics?

Early: GBS (MC)

Late: E.coli or Klebsiella

Need to get cultures for specific antibiotics so broad spectrum antibiotic is used @ start.

Problem with diagnosing neonatal pneumonias?

Have similar signs, so can be challenging to diagnose it w/ nonspecific signs and symptoms. Easy way is knowing maternal history.

Cinical presentation of neonatal pneumonia

Superimposed on RDS and they HAVE A COUGH! Baby’s normally do not cough.

ABG and CXR for neonatal pneumonia

ABG: metabolic acidosis w/ hypoxemia + hypercapnia, esp if septic then need to act fast!

CXR: varies + similar to RDS but has pleural effusions + patchy infiltrates

Neonatal pneumonia prevention (3). What are the names of the broad spectrum antibiotics (2)?

1. ampicillin and gentamicin (broad spectrum antibiotics)

2. O2 therapy w/ early NIV intervention

3. Vertical transmission of GBS (aka group B, aka from mom! Treat mom! If she has fever, concern increases!)