Mod 1 Neonatology Flashcards
1
Q
What condition is the CxR?
A
Diaphragnmatia Hernia
2
Q
What patho is usually associated with are babies who have a diaphragmatic hernia [DH]?
A
severe RDS
- the lungs can’t develop with DH
- the space is compressing the lungs
3
Q
What is congenital diaphragmatic hernia
A
A failure or malformation of the posterior lateral portion of the diaphragm prior to 8 weeks
- Abnormal opening due to closing failure or membrane hypoplasia that leaves an opening between the peritoneal and pleural spaces
- Herniation of varying amounts of intestines go into the chest compressing the chest cavity
4
Q
why is pulmonary development impaired due to pulmonary hypoplasia and pulmonary hypertension?
A
Decreased O2 delivery to the body, Leads to chronic hypoxia
- Hypoxemic vasoconstriction (impaired gas exchange and reduced O2 delivery to the body blood flow)
5
Q
What is congenital cystic adenomatoid malformation (CCAM)?
A
A rare abnormal lung development caused by a cyst or mass in the chest
6
Q
What are some clinical manifestations of congenital diaphragmatic hernia?
A
significant resp. distress at birth
- A high PVR is maintained with a persistent shunt
(recall that PVR drops and systemic pressure increases at birth) - Barrel shaped chest w/scaphoid abdomen
- Diminished or absent b/s on affected side w/hear sounds displaced
7
Q
what can you expect of oxygenation and acid-base balance when a baby has congenital diaphragmatic hernia?
A
Severe hypoxia and acidosis until the intestines are removed from the thoracic cavity
8
Q
3 reasons to use vasodilators on a baby with diaphragmatic hernia?
A
- Reduce hypertension
- Reduce afterload so the right side doesn’t need to work as hard (dilates the vessels)
- Aid Oxygenation
9
Q
what are nitric oxide (iNO) and ipprostenol used for?
A
Improve oxygenation and reduce high pulmonary vascular resistance (PVR)
- used for persistent pulmonary hypertension of the newborn (PPHN) and certain forms of pulmonary hypertension.
10
Q
how would you manage a baby w/congenital diaphragmatic hernia?
A
Intubate immediately (avoid BVM) and Insert a large OG/NG to decompress GI tract and prevent GI distension
- Ventilate w/low volumes, pressure w/higher rates (HFO)
- hyperoxygenate
- Decrease hypertension w/vasodilators
- Surgical correction after stabilization
- ECMO
11
Q
why would you use higher rates (HFO) to manage congenital diaphragmatic hernias?
A
The goal is to keep the baby alkalotic to prevent pulmonary vasospasms in the hypoplastic lung
- also avoids lung damage for is developed
12
Q
Why would you use iNO on a baby w/congenital diaphragmatic hernia?
A
To decrease pulmonary hypertension
13
Q
What is Tracheosophageal fistula?
A
Defect w/atresia of the upper esophagus w/a communication to the trachea
- basically things are connected where you don’t want it, aren’t there, or blocking
14
Q
How is the diagnosis made for tracheoesophageal fistula?
A
Made by the inability to pass a catheter into the stomach
15
Q
Atresia vs Fistula only?
A
Atresia lacks connection
Fistula is fused
There is a combo of both called
16
Q
What are some clinical manifestations of tracheoesophageal fistula (T/E)
A
- Accumulation of secretions in the mouth
- Drooling may be associated w/choking or gasping
- sporadic and/or continuous resp. distress (especially during feeding)
- Repeated regurgitation
- Increased abdominal girth w/bagging
17
Q
why don’t you want to use a BVM when managing congenital diaphragmatic hernias?
A
To avoid gastric insufflation
18
Q
How would you manage tracheoesophageal fistula?
A
- Ventilate
- Keep infant upright 30d to help decrease aspiration
- Frequent suctioning
- Broad-spectrum antibiotics
- surgical repair
19
Q
What is Pierre-Robin Syndrome?
A
TLDR: Baby basically has no chin.
- BIG TONGUE, SMALL CHIN, SHORT JAW
- Defect with mandibular hypoplasia, posterior/downward placement of the tongue, small chin, in association with cleft palate
20
Q
Why is Pierre-Robin Syndrome condition concerning?
A
The tongue is displaced bc of the lack of chin/lower jaw
- Tongue displacement causes variable amount of airway obstruction and resp. distress
21
Q
How can you manage Pierre-Robin Syndrome?
A
- Proning the baby face down might relieve obstructions
- nasotracheal tube may help patent airway
- Pt. will outgrow the problem but will require a trach/surgery
22
Q
In the brain does high CO2 lead to vasodilation or vasoconstriction of vessel tone?
A
Vasodilation
23
Q
How do we treat brain injuries with high ICP?
A
Permissive hypocapnia and iNO
- we want to decrease hypertension
24
Q
In the lungs, does high CO2 cause vasoconstriction or vasodilation?
A
If there is high CO2 in pulmonary vessels it may cause vasoconstriction
25
What is Choanal Atresia?
Defect of a blockage or absence of the posterior nares due to congenital malformation.
- Can be membranous or bony in origin
- Obstruction can be unilateral or bilateral resulting from the bony septum or soft tissue.
26
Why is a obstruction caused by atresia in the nares a problem?
Newborns are obligate nose breathers.
27
What are clinical manifestations of Choanal Atresia?
- Inability to pass suction catheter down the nares.
- Respiratory distress due to partial or total upper airway obstruction immediately after birth
28
What is the management plan for Choanal Atresia?
- Make infant cry, it causes them to breath via their mouth (initial treatment)
- Use of oral airway/intubation may help until reconstruction
29
What defects causes a decreased radius in the trachea on inspiration?
Tracheomalacia and tracheal stenosis.
- Both conditions cause a reduction in airflow due to collapse or narrow airways.
- cartilage is weak (floppy) or there is a stenotic section (narrow) of the trachea due to malformation or trauma
30
Generally, what causes a symptomatic and spontaneous pneumothorax in neos?
High inspiratory effort or secondary to the use of PPV
31
How do you manage a pneumothorax in a infant?
- observe or give 100% oxygen (nitrogen wash out)
- chest tube if pt. is on a vent
- needle the chest
32
What is Transient Tachypnea of the newborn (TTNB)?
- Pathophysiology?
A type II resp. distress syndrome known as "wet lung".
- Characterized by **Delayed fetal lung fluid reabsorption** that promotes edema (increased fluids in the lungs) or delays shunt closure.
- Benign condition of temp. resp. distress in term infants occurring hours after birth
33
Which demographic of infants is affected by Transient Tachypnea of the Newborn [TTNB]?
- C section babies bc of lack of thoracic squeeze
- baby boys
- Maternal analgesia/anethesia
- prolonged labour
34
Why are increased fluids in the lungs a problem in newborns?
- Consider TTNB
Increased fluids in the lungs cause:
- Decreased compliance and Vt.
- There is a increase in deadspace
35
What is the Apgar score and why do we use it?
Score used to evaluate overall well being of newborns immediately after birth (numerical score out of 10). It assesses:
- Appearance (babies skin color)
- Pulse (babies heart rate)
- Grimace Response
- Activity (muscle tone)
- Respiration (breathing effort)
36
Why is caesarean delivery a risk of causing Transient Tachypnea of the Newborn (TTNB)
Due to the lack of thoracic squeeze
37
When do you assess apgar?
1 minute and 5 minutes in
38
What would indicate a neonate needs reassessment?
Apgar score less than 7
39
Apgar scale?
40
How long does Transient Tachypnea of the Newborn (TTNB) last?
Usually resolves in 72 hrs. Prognosis is good
41
When does transient tachypnea of the newborn (TTNB) manifest?
Term infants who may or may not be mildly depressed at birth with good Apgars who develop tachypnea shortly after delivery, usually within 24 hours
42
Why is Choanal Atresia a problem?
Obstruction may be unilateral or bilateral from the bony septum or soft tissue.
- resp. distress can result because newborns are obligate nose breathers.
43
Meconium Aspiration Syndrome (MAS) can block air from exiting the alveoli.
- What are the consequences?
Severe resp. distress w/CO2 retention and hypoxia.
- increased PVR
- Hyperinflation of the lungs
- Ductal shunting leading to persistent fetal circulation
44
Why is persistent pulmonary hypertension linked w/meconium aspiration syndrome (MAS)
A combo of Airway obstructions, pneumonitis, surfactant inacviation and vascular remodling in MAS causes vasoconstriction in Pulmonary vascular bed causing the lungs to be poorly ventialted which resutls in hypoxia.
- **Hypoxia causes vasoconstriction** in the lungs which further **increases PVR**
- Chronic hypoxia and inflammation from MAS can lead to structural changes in the pulmonary vasculature, including thickening of the vessel walls.
45
What does the following CxR present?
Meconium Aspiration Syndrome.
- Appears as course **asymmetric pattern** w/clear infiltrates in the center.
- **Enlargement of the heart** may be secondary to fluid overload
46
If thick Mec is present and the babe is not active, what should your next steps be?
Deep suction (intubate if oral/nasal suctions fails)
- oxygen for hypoxia
- ventilation after adequate suctioning
47
With HMD/RDS, why are broken leaky capillaries a issue?
Fluid build up in the alveoli = diffusion defect
48
What are the consequences of refractory hypoxemia?
Acidosis -> increase in PVR
- With HMD/RDS, immature lungs instable/overflexible chest wall => pneumomediastinum, pneumothoraces, interstitial emphysema (PIE).
49
What would the progression of HMD/RDS look like?
- what are key things to note?
- Deals with immature lungs and increasing oxygen demand.
- surfactant deficiencies and increasing PVR = poor perfusion
50
Management for HMD/RDS?
- Oxygen, mechanical ventilation / CPAP + BIPAP, and surfactant replacement therapy are the mainstays of treatment.
- Permissive hypercapnia
51
How does permissive hypercapnia help w/HMD/RDS
HFO and iNO for high PVR and oxygenation problems.
Major complications of RDS/ HMD are pneumothoraces, oxygen toxicity, and BPD (Bronchopulmonary Dysplasia).
52
What is the progression of RDS/HMD path?
- what condition does it lead to?
Leads to BPD/CLD
53
Why are PDAs (L->R) shunts?
Increased pulmonary blood flow and prostaglandin keeps it open for fetal circulation. Lungs don't take part in O2 exchange in Fetal circulation so shunting bypasses it.
- Dependant on size of PDA
- PDAs are a defect if left open after birth, usually occurs in premies
- PaO2 stays lower for longer w/TTNB (needs fact check)
54
Management for Transient tachypnea of the Newborn (TTNB)
- Supportive care w/O2, CPAP, and diuretics (does not treat it tho)
- feeding will be stopped until resp. distress subsides
- usually resolves w/72 hrs.
55
How does a Hyperoxic test help rule out Cyanotic heart diseases?
Cyanotic = R->L shunt.
- SpO2 wouldn't increase bc mixed or deoxygenated blood is being pushed systemically.
56
What is Meconium Aspiration Syndrome (MAS)
A stressed infant in utero gets hypoxic begins shits Meconium into the amniotic fluid, the babe can then reinhale it cause its gasping from stress.
- Leads to airway obstruction and inflammation bc chemical pneumonitis.
57
Key points on the Pathophysiology of Meconium Aspiration Syndrome (MAS)
- Severity is dependent to meconium quantity in amniotic fluid
- Thick Mec, can cause total/partial airway obstruction leading to air trapping, atelectasis, hypoventilation.
- **Air leaks occur as air enters alveoli but can't exit due to check-valve effect**
Mec related airway inflammation results in: edema, surfactant dilution, exudate formation, alveolar collapse, and small airway narrowing, increasing respiratory distress
58
Why is meconium aspiration syndrome (MAS) concerning?
- snowball effect?
Leads to resp. distress w/CO2 retention -> **hypoxia** -> high PVR -> hyperinflated lungs and ductal shunting which causes **persistent fetal circulation**
59
Clinical Manifestations of Meconium Aspiration Syndrome (MAS)?
- Grunting, nasal flaring, retractions, cyanosis
- visible mec
- Dry peeling skin (mature babes)
- Visible chest diameter (air trapping)
- Crackles & Wheezing are often heard.
60
CxR findings for Meconium Aspiration Syndrome (MAS)?
- Hyperinflation
- Flattened diaphragms
- **Course irregular (asymmetric) patchy infiltrates**
- **Increased lung fluid**
- pneumothorax and pneumomediastinum may also be present
61
What would ABGs reveal about Meconium Aspiration Syndrome (MAS)?
**Acidosis**
- Babe would have mild to severe hypoxemia to hypercarbia (CO2 retention & impaired ventilation)
62
Management plan for Meconium Aspiration Syndrome (MAS)?
Basically suction if visible, if thick clear it before suction so you don't push it down.
- O2 for hypoxemia
- generally, High rates w/low volume for vents (or iNO)
63
Why are patients w/Meconium Aspiration Syndrome (MAS) hard to treat?
Pulmonary hypertension and widespread alveolar obstruction.
- ECMO is used as a last resort for (MAS)
64
Babes at risk of HMD/RDS?
- PREEMIES < 30 weeks gestation
- baby boys
- < 1200g
- birth asphyxia
- maternal complications
65
What is HMD/RDS
RDS due to immature/premature lung AND **insufficient lung surfactant**
66
When does surfactant production start?
24-28 Weeks
67
Why are immature lungs a problem when a babe develops HMD/RDS?
Distance between the alveoli and pulmonary vasculature is too great.
68
Pathophysiology of HMD/RDS: what are the main complications with this disease process?
- **Surfactant deficiency increases alveolar surface tension**
- Inability to maintain WOB needed to generate high intrathoracic pressures
- Hypoxia
- Broken leaky capillaries
- Refractory hypoxemia
69
What happens if atelectasis occurs?
Decrease in compliance which causes a decrease in compliance = Hypoxia.
- Hypoxia causes a increase in PVR and Acidosis.
- Also, V/Q mismatch
70
Clinical manifestations of HMD/RDS?
- Diminished B/S w/crackles
- Retractions, tachypnea, nasal flaring, and grunting
- See-saw abdominal breathing
- Tachycardia and refractory cyanosis
71
How long can you expect symptoms of HMD/RDS to last?
Usually resolves in 5-7days.
- symptoms peak at 72 hrs
72
What are major complications of RDS/HMD?
pneumothoraces, oxygen toxicity, and BPD (Bronchopulmonary Dysplasia).
73
What can you give to support pts. w/HMD/RDS?
HFO and Inhaled Nitric Oxide (iNO) for high PVR and oxygenation problems.
74
What is Pulmonary Interstitial Emphysema (PIE)
Air trapped in the tissues outside the alveoli caused by overdistension.
- Common in NICU babes/low birth weight babes
75
Pneumonia is usually transmitted bacterially, what is the most common type that infects perinatal and term kids?
Strep B
76
How to babes get pneumonia?
- Tranplacentally from mom to babe in utero
- perinatally via contaminated amniotic fluid
- passage through colonized vaginal tract. postnatally from exogenous sources.
77
What is the pathophysiology of pneumonia?
Alveolar infection, filling, pus formation.
- Generally speaking, **inflammation and diffusion defects**
78
What lab finding would indicate if a babe had a pneumonia?
Blood work may show signs of infection (increased leukopenia)
79
What could you expect to see on a CxR of a babe w/pneumonia.
Generally, expect white out, infiltrates, hyperinflation, and pleural effusions.
- it wouldn't be uncommon to see consolidations, bronchograms, or abscesses depending on the source of infection.
80
Management of Pneumonia for neonates/peds?
**Broad spectrum antibiotics w/fluid therapy and symptomatic control.**
- O2 therapy and ventilation may be required for severe cases.
81
What is Persistent Pulmonary Hypertension (PPHN or PFC)?
Pulmonary hypertension from failure of the PVR to fall after birth.
- keeps PDA/PFO which leads to a (L -> R) shunt
- Systemic pressures are still higher than pulmonary pressures. Blood would be shunted via PDA
82
What 4 tests are used to test for Persistent Pulmonary Hypertension (PPHN or PFC)?
- Echo (take a look)
- Hyperoxia test
- Pre and post Ductal TC test
- Pre and Post Ductal ABG
83
What is the order arteries in the ascending aorta?
ABCS!
Aorta – Brachiocephalic – L Common Carotid – L Subclavian
84
Function of Prostaglandin (PGE1)?
Keeps PDA open and dilates pulmonary vasculature
85
Function of Indomethacin
Closes PDA
86
Pathophysiology of Persistent Pulmonary Hypertension (PPHN or PFC)?
Increased PVR, causing (R -> L) shunting through the ductus arteriosus.
87
Why is Persistent Pulmonary Hypertension (PPHN or PFC) referred to as a vicious cycle
(R->L) Shunting causes:
- Decreased pulmonary return to the left side of the heart contributes to a pressure difference between the left and right sides allowing the foramen ovale to remain open
- More shunting, persistence of the severe hypoxemia (refractory), and acidosis = pulmonary vasoconstriction and reactivity, decreases pulmonary blood flow
88
Clinical manifestations of Persistent Pulmonary Hypertension (PPHN or PFC)?
- Tachypnea, mild to moderate respiratory distress with cyanosis, and hypoxemia that is **poorly responsive to oxygen therapy**
- An **audible murmur** may be present due to aortic regurgitation
89
Lab findings for Persistent Pulmonary Hypertension (PPHN or PFC)?
A-a gradient increases w/marked acidosis and severe hypoxemia.
- low volume murmur
90
Management Persistent Pulmonary Hypertension (PPHN or PFC)?
**Primary goal is to decrease PVR and increase pulmonary blood flow (increase left heart flow)**
- Ventilate to Normal PaCO2 & pH balance.
- Vasodilators to decrease PVR (Prostaglandin I)
- iNO for pulmonary vasodilation
- Restrict handling and suctioning
91
Why would you hyperoxygenate a babe w/Persistent Pulmonary Hypertension (PPHN or PFC)?
High PaO2 promots pulmonary vasodilation (HFO)
92
What is TTNB in simple terms.
A self limited condition that clears on its own, resulting from inadequate fluid clearance from the neonatal lung resulting in decreased C and increased R causing increased WOB and RR
93
What are the hallmark signs of Pulmonary Interstitial Emphysema (PIE)?
Sudden deterioration for no reason
- Poor ABGs, Compliance changes, increasing SOB, increasing vent requirments
- **Bubbling near the hilar region, radiating outward**
- Radiolucent cysts (could be linear)
94
Management for Pulmonary Interstitial Emphysema (PIE)?
Minimum vent support (prevent barotrauma)
- prone positioning or laying worst lung down to improve perfusion
- selected intubation
95
Pathophysiology of Pulmonary Interstitial Emphysema (PIE)?
- What are the consequences of air leaks?
Air can compress the interstitial and vasculature, which causes hypoxemia via:
- Decreased pulmonary perfusion
- Increasing PVR
- (R->L) Shunting
96
Where can air trapped/leaked as a result of a pulmonary interstitial emphysema (PIE) move out to and cause complications?
Interstitium
- Pneumomediastnium
- pneumopericardium
- pneumothorax.
97
What is a Hyperoxia test?
Assesses oxygenation
- FiO2 of 100% for 10 minutes with hyperventilation
- Draw an ABG
- If PaO2 is below 100 mmHg, the diagnosis is (R -> L) shunt
98
What does Pre and Post Ductal TC testing do?
Checks if there is a (R->L) shunt.
- Place TC sensors on the right upper quadrant (pre) and on the left abdomen (post)
- **If the PaO2 is higher on the right sensor by 20 mmHg or more**, there is a (R->L) shunt
99
What does Pre and Post Ductal ABG identify?
If Shunting is present.
- ABG from right radial and from UAC – greater than 20 mmHg difference, shunting is present
100
What are 3 types of Shunts?
1. Ductus Venosus - bypass liver
2. Foramen Ovale - bypass lungs
3. Ductus arteriosus - bypass l/s heart
101
Describe how oxygenated blood travels from the placenta?
102
What is Lectin (Sphingomyelin ratio) used for?
- Normal ratio?
- What does a abnormal ratio indicate?
Uses Surfactant to indicate lung maturity and amount of surfactant present based on the presecne of lectin and "S"
- The higher the ratio, the more effective surfactant is present
- should be > 2:2.5
- < 1.5 = RDS
- Test in the amniotic fluid
103
What is given to speed up lung development?
Steroids if early delivery is a risk (beclmethasone specfically!)
104
Briefly describe the main development products in the 5 stages of fetal development
1. Embryonal (day 26-52) - trachea and diaphragm formation
2. Pseudoglandular (day 52 - week 16) - conducting airways
3. Canicular (week 17- 26) - vascular bed and alveolar sacs
4. Saccular (week 26-36) - sacs grow
5. Alveolar (wee 36 - term) - alveoli develop inside sacs
105
What happens to fetal circulation after birth?
PVR drops as the lungs expand and oxygenation improves
106
What direction does blood flow in a baby with PPHN?
Blood continues to shunt (R->O) through fetal circulatory pathways (PDA or PFO) bypassing the lungs and leading to severe hypoxemia.
