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NEO REVIEW > NEO RESP > Flashcards

NEO RESP Flashcards

1
Q

what are the differentials for respiratory distress that is airway?

A

Choanal atresia
Tracheal stenosis
Laryngeal web
Vascular Ring

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2
Q

what are the differentials for respiratory distress that is thoracic?

A

Ribcage anomalies
(Jeune syndrome –
asphyxiating thoracic
dystrophy)
Air leak syndromes
Chylothorax

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3
Q

What are the differentials for respiratory distress that is of neuromuscular origin?

A

Neuromuscular
Spinal cord injury
Spinal muscular
atrophy
Phrenic nerve palsy
Myasthenia gravis
Muscular dystrophy

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4
Q

What are the differentials for respiratory distress that are nonspecific?

A

Other
Diaphragm eventration
Pain
Sepsis
Methemoglobinemia
Anemia

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5
Q

cyanotic with feeds,
with resolution during crying–> dx?

A

choanal atresia

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6
Q

what syndromes are associated with choanal atresia?

A

CHARGE association, Apert’s syndrome, DiGeorge syndrome, trisomy 18, Treacher Collins syndrome, and camptomelic dysplasia.
Approx 50% patients have other anomalies,
most commonly CHARGE syndrome

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7
Q

whats more common u/l or b/l choanal atresia?

A

u/l 2/3 and R>L
* Bilateral CA present early, more commonly
associated with other anomalies, unilateral
usually isolated

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8
Q

more choanal atresia in f vs m? or m>f?

A

F>M

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9
Q

what injury can you have that leads to respiratory distress with shoulder dystocia? waiters tip / erbs palsy

A

phrenic nerve palsy
Phrenic nerve injury – most commonly on right side after birth trauma

  • Etiology – lateral neck
    hyperextension at birth, affects
    C3‐C5
  • Approximately 75% have
    associated injuries (brachial
    plexus, Horner’s)
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10
Q

what does the cxr show with phrenic nerve palsy?

A

CXR with elevated hemidiaphragm with atelectasis
* Fluoroscopy diagnostic – paradoxical
movement of diaphragm – elevation with inspiration, descent with expiration
* Improvement over 2‐3 weeks, further over next few months
* If failure of improvement in respiratory status, may require diaphragm plication

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11
Q

what kind of nerve injury with breech with neck hyperextension?

A

spinal cord injury

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12
Q

brainstem injury what happens?
at or above c3?
Below C3?

A

Level of injury:
* Brain stem – can be fatal
* At or above C3 – phrenic nerve is also involved
* Below this level – Phrenic nerve is intact and diaphragm contracts vigorously to compensate for weak intercostal and abdominal muscles

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13
Q
  • Vigorous use of diaphragmatic muscles in a hypotonic infant – rule out what?
A
  • Vigorous use of diaphragmatic muscles in a hypotonic infant – rule out spinal cord injury
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14
Q

decreased risk for
development of pneumothorax?

A

Surfactant admin vs
Positive pressure ventilation
Frequent suctioning
Prematurity

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15
Q

incidence of ptx?
Risk factors?
when does a ptx usually resolve?

A

Pneumothorax
* Spontaneous pneumothorax in ~1‐2% of live births
* Risk factors include meconium aspiration, respiratory
distress syndrome, pulmonary hypoplasia
* Usually resolve in 1‐2 days

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16
Q

what is the sail sign, when do you see it?

A

Pneumomediastinum
* ‘sail sign’ – elevation of thymus from pericardial silhouette

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17
Q

heart sounds, pericardial rub, narrow pulse pressure - dx?

A

pneumopericardium

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18
Q

PIE - what causes it?
seen mostly in?
Is it diffuse? b/l?

A

Alveolar overdistension leading to rupture
* Primarily seen in premature ventilated patients
* Diffuse bilateral disease
* Localized – one or more lobes and mediastinal shift

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19
Q

You are passing by the bedside for a newborn infant on CPAP respiratory
distress and hear biphasic stridor as they are changing the mask.
Respiratory status worsens and stridor becomes louder. What is the most likely etiology?

A

Subglottic stenosis

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20
Q

inspiratory stridor due to what type of obstruction?

A

Inspiratory

Extrathoracic or upper airway obstruction
Large tongue, laryngomalacia, laryngeal cyst, congenital

tracheal stenosis (tracheal rings)

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21
Q

biphasic stridor due to what type of obstruction?

A

Biphasic
Glottic or subglottic

Subglottic stenosis, subglottic hemangioma

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22
Q

expiratory stridor due to what type of obstruction?

A

Expiratory
Intrathoracic airway obstruction
Arch anomalies, vascular rings, tracheomalacia of intrathoracic
segment of trachea

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23
Q

Most common cause of inspiratory stridor in a neonate?

A

Laryngomalacia

24
Q

what are pulmonary causes of respiratory distress?

A

Acquired Pulmonary etiology
* Transient Tachypnea of the Newborn
* Pneumonia
* Pneumothorax
* Meconium aspiration syndrome

Congenital malformations of the lung
* Congenital Pulmonary airway malformation
* Congenital Pulmonary lymphangiectasia
* Congenital lobar emphysema
* Mediastinal tumors

25
Q

what congenital anomalies happen during the embryonic phase?

A

TE fistula, pulm sequestration,
cong lobar emphysema

26
Q

what congenital anomalies happen during the Pseudoglandular phase?

A

CDH, CPAM, bronch cyst,
bronchopulm sequestration

27
Q

what congenital anomalies happen during the canicular phase?

A

RDS, alveolar capillary dysplasia, pulmonary hypoplasia

28
Q

what congenital anomalies happen during the saccular phase?

A

RDS, BPD, pulmonary
hypoplasia

29
Q

what congenital anomalies happen during the alveolar phase?

A

TTN, MAS, pneumonia, PPHN,
emphysema

30
Q

A full‐term neonate is delivered by c‐section, and demonstrates tachypnea,
grunting, and hypoxemia necessitating NICU care. At birth, activation of which
intracellular channel aids in reabsorption of lung fluid?

A

Epithelial sodium channels

31
Q

fetal lung fluid - how much is made towards end of gestation?

A

30‐50ml/kg fluid in fetal lamb lungs towards end of
gestation

  • Fetal lung fluid encompasses 90‐95% total lung weight toward term, decreases few days prior to delivery
32
Q

what ion does the pulmonary epithelium secrete into the alveoli? what ion follows?

A
  • Pulmonary epithelium secretes chloride into alveoli
  • Na follows Cl through paracellular pathways, maintaining lung fluid
33
Q

labor onset what happens in lung with fluid?

A

Labor onset leads to increased circulating epinephrine,
stimulating epithelial sodium channels (ENaC)

Na moves into interstitium through Na/K channels with
chloride and water passively following

  • Fluid then passes to pulmonary circulation primarily, lymphatics secondary

Fluid also exits via squeeze of thorax during vaginal birth

34
Q

what are the risk factors for TTN?

A

C Section, maternal Diabetes, male sex, macrosomia, maternal asthma, delivery of preemie or late preterm

35
Q

Incidence of TTN at 33-34 wga, 35 - 36 wga, and in term?

A

Incidence: 3.6‐5.7/1000 births
* 10% pts 33‐34wks
* 5% pts 35‐36wks
* 1% term infants

36
Q

Symptoms within first 6 hours of delivery
* Tachypnea, grunting
Dx?

A

TTN

37
Q

imaging in ttn shows?

A

Imaging
* Fluid in fissure
* Perihilar streaking
* Congestion

38
Q

mx of ttn and when does it resolve?

A

Management
* Oxygen supplementation, positive pressure support
* Usually resolves by 48‐72 hours

39
Q

Chylothorax - which is more common congenital or acquired? what syndromes are the congenital assoc with?

A

10% Primary/Congenital – Trisomy 21, Noonan’s, Turner

90% Secondary/Acquired –most commonly
associated with thoracic surgery,
other associations include venous
thrombosis leading to increased SVC
pressure

M> F

40
Q

how many newborns with chylothorax are sx within 24 hrs and how many within 7 days?

A

50% within 24 hrs
75% within 7 days

41
Q

how to dx chylothorax?

A

Fluid cell count >
1000 μL
Lymph >80%
TG >110 mg/dL
Pleural fluid: serum cholesterol < 1

42
Q

how to mx chylothorax? when does it resolve?

A

Supportive, may take 4‐6 weeks for resolution, up to 80% will resolve
without surgery

  • Fat free diet utilizing medium chain triglycerides (MCT) – absorbed by
    portal venous system
  • Will need essential fatty acids if prolonged utilization of MCT
  • If persistent, surgical options include pleurodesis, thoracic duct ligation,
    pleuroperitoneal shunt
43
Q

Dilation of lymphatics that
results in obstruction and fluid leakage - what is dx?

A

Congenital Pulmonary Lymphangiectasia (CPL)

44
Q

what is secondary congenital pulmonary lymphangiectasia associated with?

A

Secondary CPL
Associated with cardiac defects – total anomalous pulmonary
venous return, hypoplastic left heart syndrome with restricted
atrial septum

45
Q

what is primary congenital pulmonary lymphangiectasia associated with?

A

Associated with Noonan’s, Ehlers‐Danlos, Ullrich‐Turner,
Down’s syndrome

46
Q

how does primary CPL happen?

A

Failure in development of lymphatics – starts to develop in 6th
week and lymphatic channels develop before 20 weeks
* Localized vs general lymphatic development defect
* Generalized tends to have less severe pulmonary
involvement

47
Q

Respiratory failure, hypoxia at birth, often with chylothorax, hyperinflation seen in what dx? what are the differentials?

A

CPL
differentials:
On differential in a fetal patient with non‐immune hydrops and congenital chylothorax

48
Q

congenital pna what bugs?
Early pna happens at what days? late pna at what days of life?
what bugs?

A

Congenital
– Herpes simplex, usually acquired during labor; disseminated HSV results in pneumonia in
approximately 33‐54%.

Early (1st 3‐7 days),– Group B streptococcus, E coli increasing

Late late (after 7 days of life)– RSV most common viral cause of late‐ onset pneumonia

49
Q

systemic disease + pna what bugs?

A

Systemic Disease + Pneumonia – consider CMV, HSV, toxoplasma, disseminated candida (particularly
in preterm)

50
Q

what is the pathophysiology of pna? both cellular and inflammatory

A

Cellular Injury
Alveolar surface impairment leading to
transudation of fluid (pulmonary edema), surfactant impairment

Inflammatory response
* Neutrophil recruitment
* Bacterial and inflammatory debris leading to airway obstruction
* Increases in pulmonary vascular resistance through vasoconstrictor and procoagulants

bacterial toxin exposure or Viral exposure – CMV and HSV infection
leads to lysis of pneumocytes,
further viral growth
lead to cellular injury and inflamm response

51
Q

what is the cdc definition of pna?

A

Signs/Symptoms in infants <1year old:
Worsening Gas Exchange (Desats, increased vent settings)

+ 3 of the following:
* Temperature instability
* Leukopenia (≤4000 WBC/mm3 ) or leukocytosis (>15,000 WBC/mm3 ) and left shift (>10% band forms)
* New onset of purulent sputum or change in character of sputum , or increased respiratory secretions or increased suctioning requirements
* Apnea, tachypnea, nasal flaring with retraction of chest wall or nasal flaring with grunting
* Wheezing, rales, or rhonchi
* Cough
* Bradycardia (<100 beats/min) or tachycardia (>170 beats/min)

52
Q

what will imaging show with pna?

A

Imaging:
With underlying pulmonary
or cardiac disease:

2 or more CXR with:
New and persistent or
Progressive and persistent
Infiltrate, consolidation,
cavitation or pneumatocele
*IF no underlying pulm or
CV disease, can diagnose
from 1 xray

53
Q

You are called to a csection for a fetus with prenatal diagnosis of congenital lung malformation. Baby delivers via NSVD and is initially vigorous, crying, begins to quiet, and HR <100. Baby is then intubated and brought to NICU. Which is the most common type of congenital pulmonary airway malformation?

A

Type 1 – Macrocystic (cysts > 2cm)

Incidence
Rare, approximately 1/10000‐1/35000 live births

Types
* Congenital pulmonary airway malformation (CPAM) – 40%
* Bronchopulmonary sequestration (BPS) – 10%
* Congenital lobar emphysema (CLE)
* Bronchogenic cysts (BC)

Most common time for detection is a fetal
ultrasound – many asymptomatic in the neonatal

54
Q

pulmonary sequestration happens in what phase of lung dev?

A

embryonic (pulm sequestration, TE fistula, congenital lobar emphysema)

55
Q

cpam in what phase of lung dev?

A

pseudoglandular (cdh, cpam, bronchogenic cyst)

56
Q

what is the pathophys of cpam?

A

Pathophysiology
Malformation during pseudoglandular stage
Macrocystic lesions (>5mm) better prognosis than microcystic (<5mm)

Most often found in lower lobes,
right = left

57
Q
A

NEO REVIEW (3 decks)

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