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Patho 2 (Path 311) > Mod 1 Neonatology > Flashcards

Mod 1 Neonatology Flashcards

1
Q

What condition is the CxR?

A

Diaphragnmatia Hernia

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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
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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
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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)
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5
Q

What is congenital cystic adenomatoid malformation (CCAM)?

A

A rare abnormal lung development caused by a cyst or mass in the chest

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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
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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

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8
Q

3 reasons to use vasodilators on a baby with diaphragmatic hernia?

A
  1. Reduce hypertension
  2. Reduce afterload so the right side doesn’t need to work as hard (dilates the vessels)
  3. Aid Oxygenation
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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.
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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
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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
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12
Q

Why would you use iNO on a baby w/congenital diaphragmatic hernia?

A

To decrease pulmonary hypertension

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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
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14
Q

How is the diagnosis made for tracheoesophageal fistula?

A

Made by the inability to pass a catheter into the stomach

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15
Q

Atresia vs Fistula only?

A

Atresia lacks connection

Fistula is fused

There is a combo of both called

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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
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17
Q

why don’t you want to use a BVM when managing congenital diaphragmatic hernias?

A

To avoid gastric insufflation

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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
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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
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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
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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
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22
Q

In the brain does high CO2 lead to vasodilation or vasoconstriction of vessel tone?

A

Vasodilation

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23
Q

How do we treat brain injuries with high ICP?

A

Permissive hypocapnia and iNO

  • we want to decrease hypertension
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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

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25
Q

What is Choanal Atresia?

A

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.
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26
Q

Why is a obstruction caused by atresia in the nares a problem?

A

Newborns are obligate nose breathers.

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27
Q

What are clinical manifestations of Choanal Atresia?

A
  • Inability to pass suction catheter down the nares.
  • Respiratory distress due to partial or total upper airway obstruction immediately after birth
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28
Q

What is the management plan for Choanal Atresia?

A
  • Make infant cry, it causes them to breath via their mouth (initial treatment)
  • Use of oral airway/intubation may help until reconstruction
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29
Q

What defects causes a decreased radius in the trachea on inspiration?

A

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
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30
Q

Generally, what causes a symptomatic and spontaneous pneumothorax in neos?

A

High inspiratory effort or secondary to the use of PPV

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31
Q

How do you manage a pneumothorax in a infant?

A
  • observe or give 100% oxygen (nitrogen wash out)
  • chest tube if pt. is on a vent
  • needle the chest
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32
Q

What is Transient Tachypnea of the newborn (TTNB)?

  • Pathophysiology?
A

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
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33
Q

Which demographic of infants is affected by Transient Tachypnea of the Newborn [TTNB]?

A
  • C section babies bc of lack of thoracic squeeze
  • baby boys
  • Maternal analgesia/anethesia
  • prolonged labour
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34
Q

Why are increased fluids in the lungs a problem in newborns?
- Consider TTNB

A

Increased fluids in the lungs cause:

  • Decreased compliance and Vt.
  • There is a increase in deadspace
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35
Q

What is the Apgar score and why do we use it?

A

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)
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36
Q

Why is caesarean delivery a risk of causing Transient Tachypnea of the Newborn (TTNB)

A

Due to the lack of thoracic squeeze

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37
Q

When do you assess apgar?

A

1 minute and 5 minutes in

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38
Q

What would indicate a neonate needs reassessment?

A

Apgar score less than 7

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39
Q

Apgar scale?

A
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40
Q

How long does Transient Tachypnea of the Newborn (TTNB) last?

A

Usually resolves in 72 hrs. Prognosis is good

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41
Q

When does transient tachypnea of the newborn (TTNB) manifest?

A

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

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42
Q

Why is Choanal Atresia a problem?

A

Obstruction may be unilateral or bilateral from the bony septum or soft tissue.

  • resp. distress can result because newborns are obligate nose breathers.
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43
Q

Meconium Aspiration Syndrome (MAS) can block air from exiting the alveoli.

  • What are the consequences?
A

Severe resp. distress w/CO2 retention and hypoxia.

  • increased PVR
  • Hyperinflation of the lungs
  • Ductal shunting leading to persistent fetal circulation
44
Q

Why is persistent pulmonary hypertension linked w/meconium aspiration syndrome (MAS)

A

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
Q

What does the following CxR present?

A

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
Q

If thick Mec is present and the babe is not active, what should your next steps be?

A

Deep suction (intubate if oral/nasal suctions fails)

  • oxygen for hypoxia
  • ventilation after adequate suctioning
47
Q

With HMD/RDS, why are broken leaky capillaries a issue?

A

Fluid build up in the alveoli = diffusion defect

48
Q

What are the consequences of refractory hypoxemia?

A

Acidosis -> increase in PVR

  • With HMD/RDS, immature lungs instable/overflexible chest wall => pneumomediastinum, pneumothoraces, interstitial emphysema (PIE).
49
Q

What would the progression of HMD/RDS look like?
- what are key things to note?

A
  • Deals with immature lungs and increasing oxygen demand.
  • surfactant deficiencies and increasing PVR = poor perfusion
50
Q

Management for HMD/RDS?

A
  • Oxygen, mechanical ventilation / CPAP + BIPAP, and surfactant replacement therapy are the mainstays of treatment.
  • Permissive hypercapnia
51
Q

How does permissive hypercapnia help w/HMD/RDS

A

HFO and iNO for high PVR and oxygenation problems.

Major complications of RDS/ HMD are pneumothoraces, oxygen toxicity, and BPD (Bronchopulmonary Dysplasia).

52
Q

What is the progression of RDS/HMD path?
- what condition does it lead to?

A

Leads to BPD/CLD

53
Q

Why are PDAs (L->R) shunts?

A

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
Q

Management for Transient tachypnea of the Newborn (TTNB)

A
  • 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
Q

How does a Hyperoxic test help rule out Cyanotic heart diseases?

A

Cyanotic = R->L shunt.
- SpO2 wouldn’t increase bc mixed or deoxygenated blood is being pushed systemically.

56
Q

What is Meconium Aspiration Syndrome (MAS)

A

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
Q

Key points on the Pathophysiology of Meconium Aspiration Syndrome (MAS)

A
  • 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
Q

Why is meconium aspiration syndrome (MAS) concerning?

  • snowball effect?
A

Leads to resp. distress w/CO2 retention -> hypoxia -> high PVR -> hyperinflated lungs and ductal shunting which causes persistent fetal circulation

59
Q

Clinical Manifestations of Meconium Aspiration Syndrome (MAS)?

A
  • Grunting, nasal flaring, retractions, cyanosis
  • visible mec
  • Dry peeling skin (mature babes)
  • Visible chest diameter (air trapping)
  • Crackles & Wheezing are often heard.
60
Q

CxR findings for Meconium Aspiration Syndrome (MAS)?

A
  • Hyperinflation
  • Flattened diaphragms
  • Course irregular (asymmetric) patchy infiltrates
  • Increased lung fluid
  • pneumothorax and pneumomediastinum may also be present
61
Q

What would ABGs reveal about Meconium Aspiration Syndrome (MAS)?

A

Acidosis
- Babe would have mild to severe hypoxemia to hypercarbia (CO2 retention & impaired ventilation)

62
Q

Management plan for Meconium Aspiration Syndrome (MAS)?

A

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
Q

Why are patients w/Meconium Aspiration Syndrome (MAS) hard to treat?

A

Pulmonary hypertension and widespread alveolar obstruction.

  • ECMO is used as a last resort for (MAS)
64
Q

Babes at risk of HMD/RDS?

A
  • PREEMIES < 30 weeks gestation
  • baby boys
  • < 1200g
  • birth asphyxia
  • maternal complications
65
Q

What is HMD/RDS

A

RDS due to immature/premature lung AND insufficient lung surfactant

66
Q

When does surfactant production start?

A

24-28 Weeks

67
Q

Why are immature lungs a problem when a babe develops HMD/RDS?

A

Distance between the alveoli and pulmonary vasculature is too great.

68
Q

Pathophysiology of HMD/RDS: what are the main complications with this disease process?

A
  • Surfactant deficiency increases alveolar surface tension
  • Inability to maintain WOB needed to generate high intrathoracic pressures
  • Hypoxia
  • Broken leaky capillaries
  • Refractory hypoxemia
69
Q

What happens if atelectasis occurs?

A

Decrease in compliance which causes a decrease in compliance = Hypoxia.

  • Hypoxia causes a increase in PVR and Acidosis.
  • Also, V/Q mismatch
70
Q

Clinical manifestations of HMD/RDS?

A
  • Diminished B/S w/crackles
  • Retractions, tachypnea, nasal flaring, and grunting
  • See-saw abdominal breathing
  • Tachycardia and refractory cyanosis
71
Q

How long can you expect symptoms of HMD/RDS to last?

A

Usually resolves in 5-7days.
- symptoms peak at 72 hrs

72
Q

What are major complications of RDS/HMD?

A

pneumothoraces, oxygen toxicity, and BPD (Bronchopulmonary Dysplasia).

73
Q

What can you give to support pts. w/HMD/RDS?

A

HFO and Inhaled Nitric Oxide (iNO) for high PVR and oxygenation problems.

74
Q

What is Pulmonary Interstitial Emphysema (PIE)

A

Air trapped in the tissues outside the alveoli caused by overdistension.

  • Common in NICU babes/low birth weight babes
75
Q

Pneumonia is usually transmitted bacterially, what is the most common type that infects perinatal and term kids?

A

Strep B

76
Q

How to babes get pneumonia?

A
  • Tranplacentally from mom to babe in utero
  • perinatally via contaminated amniotic fluid
  • passage through colonized vaginal tract. postnatally from exogenous sources.
77
Q

What is the pathophysiology of pneumonia?

A

Alveolar infection, filling, pus formation.

  • Generally speaking, inflammation and diffusion defects
78
Q

What lab finding would indicate if a babe had a pneumonia?

A

Blood work may show signs of infection (increased leukopenia)

79
Q

What could you expect to see on a CxR of a babe w/pneumonia.

A

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
Q

Management of Pneumonia for neonates/peds?

A

Broad spectrum antibiotics w/fluid therapy and symptomatic control.

  • O2 therapy and ventilation may be required for severe cases.
81
Q

What is Persistent Pulmonary Hypertension (PPHN or PFC)?

A

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
Q

What 4 tests are used to test for Persistent Pulmonary Hypertension (PPHN or PFC)?

A
  • Echo (take a look)
  • Hyperoxia test
  • Pre and post Ductal TC test
  • Pre and Post Ductal ABG
83
Q

What is the order arteries in the ascending aorta?

A

ABCS!
Aorta – Brachiocephalic – L Common Carotid – L Subclavian

84
Q

Function of Prostaglandin (PGE1)?

A

Keeps PDA open and dilates pulmonary vasculature

85
Q

Function of Indomethacin

A

Closes PDA

86
Q

Pathophysiology of Persistent Pulmonary Hypertension (PPHN or PFC)?

A

Increased PVR, causing (R -> L) shunting through the ductus arteriosus.

87
Q

Why is Persistent Pulmonary Hypertension (PPHN or PFC) referred to as a vicious cycle

A

(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
Q

Clinical manifestations of Persistent Pulmonary Hypertension (PPHN or PFC)?

A
  • 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
Q

Lab findings for Persistent Pulmonary Hypertension (PPHN or PFC)?

A

A-a gradient increases w/marked acidosis and severe hypoxemia.

  • low volume murmur
90
Q

Management Persistent Pulmonary Hypertension (PPHN or PFC)?

A

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
Q

Why would you hyperoxygenate a babe w/Persistent Pulmonary Hypertension (PPHN or PFC)?

A

High PaO2 promots pulmonary vasodilation (HFO)

92
Q

What is TTNB in simple terms.

A

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
Q

What are the hallmark signs of Pulmonary Interstitial Emphysema (PIE)?

A

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
Q

Management for Pulmonary Interstitial Emphysema (PIE)?

A

Minimum vent support (prevent barotrauma)

  • prone positioning or laying worst lung down to improve perfusion
  • selected intubation
95
Q

Pathophysiology of Pulmonary Interstitial Emphysema (PIE)?

  • What are the consequences of air leaks?
A

Air can compress the interstitial and vasculature, which causes hypoxemia via:

  • Decreased pulmonary perfusion
  • Increasing PVR
  • (R->L) Shunting
96
Q

Where can air trapped/leaked as a result of a pulmonary interstitial emphysema (PIE) move out to and cause complications?

A

Interstitium
- Pneumomediastnium
- pneumopericardium
- pneumothorax.

97
Q

What is a Hyperoxia test?

A

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
Q

What does Pre and Post Ductal TC testing do?

A

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
Q

What does Pre and Post Ductal ABG identify?

A

If Shunting is present.

  • ABG from right radial and from UAC – greater than 20 mmHg difference, shunting is present
100
Q

What are 3 types of Shunts?

A
  1. Ductus Venosus - bypass liver
  2. Foramen Ovale - bypass lungs
  3. Ductus arteriosus - bypass l/s heart
101
Q

Describe how oxygenated blood travels from the placenta?

A
102
Q

What is Lectin (Sphingomyelin ratio) used for?

  • Normal ratio?
  • What does a abnormal ratio indicate?
A

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
Q

What is given to speed up lung development?

A

Steroids if early delivery is a risk (beclmethasone specfically!)

104
Q

Briefly describe the main development products in the 5 stages of fetal development

A
  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
Q

What happens to fetal circulation after birth?

A

PVR drops as the lungs expand and oxygenation improves

106
Q

What direction does blood flow in a baby with PPHN?

A

Blood continues to shunt (R->O) through fetal circulatory pathways (PDA or PFO) bypassing the lungs and leading to severe hypoxemia.

Patho 2 (Path 311) (15 decks)

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