Newborn Flashcards
1
Q
What are the most common reasons for admission to a neonatal intensive care unit (NICU)?
A
Respiratory disorders
Major source of neonatal mortality and morbidity.
2
Q
What must the newborn do within the first minute of life?
A
Clear fetal lung fluid and establish gas exchange.
3
Q
At what gestational age is fetal breathing detected?
A
12–14 weeks GA.
4
Q
What are the characteristics of fetal breathing during active sleep?
A
Irregular breathing pattern (20–30 bpm) with long inspiratory and expiratory times.
5
Q
What do central chemoreceptors in the fetus respond to?
A
- Hypoxia – decreased breathing
- Hypercarbia – increased breathing and initiation of active sleep.
6
Q
What is the effect of prostaglandin E2 on fetal breathing?
A
Stops breathing.
7
Q
What combination of factors leads to rapid onset of regular breathing at birth?
A
- Removal of prostaglandin production from placenta
- Tactile and cold stimuli
- Activation of Hering-Breuer reflexes
- Changes in arterial blood oxygenation levels (PaO2).
8
Q
What percentage of term infants begin spontaneous breathing by 10–30 seconds of life?
A
85%.
9
Q
What is the function of fetal lung fluid?
A
Essential for normal lung growth.
10
Q
How is fetal lung fluid secreted?
A
By active transport of chloride by airway epithelium.
11
Q
What happens to fetal lung fluid volume as pregnancy approaches term?
A
The rate of liquid formation and volume decreases.
12
Q
How is fetal lung fluid cleared from the airways at birth?
A
- Active transport of sodium by epithelial sodium channels (ENaCs)
- Mechanical forces during birthing process
- Newborn breathing after birth.
13
Q
What is primary apnea?
A
Occurs in newborns after birth and often responds to tactile stimulation.
14
Q
What should be the initial resuscitation method for term infants?
A
Room air (21%) is preferable to 100% oxygen.
15
Q
What is secondary apnea?
A
Occurs if the infant in primary apnea is not assisted and hypoxia continues.
16
Q
What is the recommended action if an infant’s heart rate is not greater than 100 after 30 seconds of PPV?
A
Progress through a series of ventilation corrective steps (MR.SOPA).
17
Q
How should intubation be confirmed?
A
- Chest rise
- Condensate in ET tube
- Improved HR
- Carbon dioxide detector (PediCap).
18
Q
What is the appropriate action if there is no heart rate and Apgar score is 0 after 10 minutes of resuscitation?
A
Discontinue further resuscitation.
19
Q
What is the resuscitation recommendation for preterm infants born less than 32 weeks?
A
Monitor closely due to increased newborn morbidities.
20
Q
What effect do antenatal steroids have on preterm infants?
A
Improve response to resuscitation.
21
Q
What is the role of prolonged inspiratory times in resuscitation?
A
Used to overcome resistance created by air-fluid interfaces in small airways.
22
Q
What are the components of the respiratory control system?
A
- Respiratory neurons in the medulla and pons
- Pre-Bötzinger complex.
- Stretch receptors in the lungs and airways.
23
Q
What neurotransmitter activates receptors involved in generating respiratory rhythms?
A
Glutamate.
24
Q
Where are central chemoreceptors located?
A
Near the ventral surface of the medulla.
25
What happens to the respiratory response of the newborn to hypoxia?
Biphasic response with transient increase in minute ventilation followed by a decrease.
26
What is the effect of hyperoxia on breathing?
Causes temporary suppression of breathing.
27
What is the slope of ventilatory response to carbon dioxide in term infants during active sleep?
Less than during quiet sleep.
28
What is the response of the fetus to hypoxia?
Suppression of ventilation.
29
What is the biphasic response to hypoxia in newborns?
Transient increase in minute ventilation followed by a decrease to or below baseline levels.
30
What effect does exposure to hyperoxia have on breathing?
Temporary suppression of breathing due to withdrawal of peripheral chemoreceptor drive
## Footnote
After a few minutes, ventilation increases due to hyperoxic cerebral vasoconstriction resulting in increased brain tissue carbon dioxide.
31
How does immaturity and prolonged exposure to supplementary oxygen affect the response to hyperoxia?
Reduces the response to hyperoxia
## Footnote
This is particularly notable in fetuses and newborns.
32
What is the response of the fetus and newborn to increased carbon dioxide levels?
Increase in breathing activity.
33
How does the slope of ventilatory response to carbon dioxide differ in term infants during active versus quiet sleep?
Less during active sleep, but increases with postnatal growth.
34
What are subepithelial chemoreceptors and where are they located?
Located in the trachea, bronchi, and bronchioles; respond to toxic gases by changing the frequency and depth of respiration.
35
What are the three respiratory reflexes described by Hering and Breuer?
* Inflation
* Expiratory
* Deflation
36
What does the Hering-Breuer inflation reflex do?
Stimulated by lung inflation, resulting in cessation of respiratory activity.
37
What is the role of the Head’s paradoxical reflex?
Underlying mechanism of the first breath and sighing; stimulates stronger diaphragmatic contraction.
38
What does the rapid chest wall distortion via the intercostal phrenic inhibitory reflex result in?
Shortening of inspiratory efforts.
39
What protects the airway from bronchospasm induced by cold exposure?
Upper airway reflexes that increase upper airway resistance and decrease inspiratory airflow.
40
Define apnea.
Cessation of breathing for at least 20 seconds or at least 10 seconds if associated with oxygen desaturation or bradycardia.
41
What are the classifications of apnea?
* Central (46%–69%)
* Obstructive (6%–12%)
* Mixed (20%–44%)
42
What characterizes central apnea?
Cessation of inspiratory efforts in the absence of upper airway obstruction.
43
What can occur within a few seconds of onset of apnea?
Bradycardia with accompanying disturbances in blood pressure and cerebral blood flow velocity.
44
What is the incidence of apnea of prematurity related to?
Inversely associated with gestational age (GA).
45
Which pharmacologic agents can cause apnea?
* Benzodiazepines
* Opioid analgesics
46
What is the preferred agent for reducing apnea in preterm infants?
Caffeine.
47
What are the side effects of theophylline?
* Hyperactivity
* Tachycardia
* Cardiac dysrhythmias
* Feeding intolerance
* Seizures
48
What is periodic breathing and how is it defined?
Defined as 3 episodes of apnea of more than 3 seconds duration each, interrupted by periods of breathing that are 20 seconds or less.
49
What is Respiratory Distress Syndrome (RDS) also known as?
Hyaline membrane disease or respiratory instability of prematurity.
50
What is the typical presentation of RDS in preterm infants?
Develop oxygen requirements within 6 hours of life; typically require respiratory support at 24 hours of life.
51
What does the incidence of RDS decrease with?
Increasing gestational age (GA).
52
What are the classic CXR findings in RDS?
Ground-glass appearance with air bronchograms.
53
What role do surfactant proteins play in lung function?
They stabilize phospholipid monolayer and contribute to host defense.
54
What is the lecithin to sphingomyelin (L:S) ratio used for?
Assessing lung maturity; lower ratio indicates higher likelihood of developing RDS.
55
What is the consequence of an immature surfactant system in preterm infants?
Difficulty in generating a functional residual capacity (FRC) and increased work of breathing.
56
What happens during the first 24–36 hours if exogenous surfactant is not given?
Symptoms worsen due to collapse of recruited alveoli and deactivation of surfactant.
57
What is the normal range for functional residual capacity (FRC)?
25-30 ml/kg.
58
What is the relationship between fetal cortisol and lung maturation?
Fetal cortisol stimulates lung maturation.
59
What clinical findings are associated with RDS?
* Tachypnea (respiratory rate > 60 breaths/min)
* Intercostal and subcostal retraction
* Nasal flaring
* Abdominal breathing
60
What is the significance of an expiring grunt in infants with RDS?
An attempt to increase FRC.
61
What is the typical outcome for infants with RDS after endogenous surfactant production increases?
Recovery from RDS with decreasing oxygen requirements normally occurs by approximately 1 week of age.
62
What is the lamellar body count used for?
Assessing lung maturity; >37,000 correlates well with lung maturity.
63
What is a differential diagnosis for RDS?
* Severe early onset sepsis or pneumonia
* Pulmonary hypertension
* TTN
* Neonatal pneumonia
64
What is the diagnostic procedure used for preductal and postductal pulse-oximetry?
Echocardiography
## Footnote
This procedure helps assess oxygen saturation levels in different parts of the body.
65
What is the primary treatment for respiratory distress syndrome (RDS) in neonates?
Sedation and inhaled nitric oxide (iNO)
## Footnote
These treatments help manage symptoms and improve respiratory function.
66
How does Transient Tachypnea of the Newborn (TTN) typically differ from RDS?
TTN typically improves more quickly as the excessive water in the lungs is absorbed and surfactant function improves
## Footnote
TTN often resolves within a few days.
67
What is the typical onset time for neonatal pneumonia symptoms?
After 4–6 hours of age
## Footnote
This timing helps differentiate it from other respiratory conditions.
68
What are the principles of management for RDS?
* Use of CPAP to maintain alveolar distention
* Giving exogenous surfactant
* Mechanical ventilation and administration of surfactant therapy
## Footnote
These principles help bridge the time until the infant develops sufficient endogenous surfactant.
69
What is minimally invasive surfactant therapy (MIST)?
Involves direct visualization of vocal cords and insertion of a feeding tube into the upper trachea for surfactant instillation
## Footnote
This method is designed to be less invasive while delivering surfactant.
70
What is the recommended surfactant dose for neonates?
Single dose of 100 mg/kg surfactant, though better results are obtained with more than one dose
## Footnote
Multiple doses can improve outcomes in neonates.
71
What does PPV stand for and when might it be necessary in preterm infants?
Positive Pressure Ventilation; may be needed due to poor respiratory drive or inability to maintain chest expansion
## Footnote
This is critical for infants with surfactant deficiency or respiratory muscle weakness.
72
True or False: NIPPV has been shown to reduce the incidence of extubation failure.
True
## Footnote
However, it had no effect on bronchopulmonary dysplasia (BPD) or mortality.
73
What are some benefits of volume ventilation compared to pressure ventilation in preterm infants?
* Reduced death or BPD
* Shorter duration of ventilation
* Fewer pneumothoraces
* Decreased severe intraventricular hemorrhage
## Footnote
Volume ventilation allows for rapid adjustments in inspiratory pressures.
74
What is the role of antenatal steroids in respiratory management?
Mature fetal lung and brain, decrease fetal lung fluid, induce surfactant production
## Footnote
Dexamethasone and betamethasone are commonly used.
75
What is the mortality rate associated with RDS?
5%–10% overall; inversely proportional to gestational age (GA)
## Footnote
Antenatal steroids and surfactant therapy have decreased mortality rates.
76
What are some risk factors for Transient Tachypnea of the Newborn (TTN)?
* C-section birth
* Male sex
* Macrosomia
* Maternal diabetes
* Maternal history of asthma
## Footnote
These factors increase the likelihood of TTN occurring.
77
What causes TTN at birth?
Ineffective clearance of fetal lung fluid
## Footnote
Conditions like elective cesarean section contribute to this problem.
78
What is the typical clinical presentation of TTN?
* Tachypnea
* Hyperinflated chest
* Less frequent grunting
## Footnote
These signs help differentiate TTN from other respiratory issues.
79
What should be considered in the management of TTN?
* Supplemental oxygen
* CPAP
* IV antimicrobials if sepsis is suspected
## Footnote
Most cases improve significantly within 24 hours.
80
What is Meconium Aspiration Syndrome (MAS) associated with?
* Advanced gestational age
* Low Apgar scores
* C-section delivery
## Footnote
These factors increase the risk of MAS.
81
What is the pathophysiology of Meconium Aspiration Syndrome?
Inflammatory lung condition caused by aspiration of meconium-stained amniotic fluid during delivery
## Footnote
This can lead to airway obstruction and impaired surfactant function.
82
What are the initial chest radiograph findings in MAS?
* Hyperinflated lung fields
* Widespread patchy infiltrates
## Footnote
These findings help in diagnosing MAS.
83
What is the recommended management for infants with MAS?
* Supplemental oxygen to keep O2 saturation >94%
* Consider mechanical ventilation if high FiO2 is needed
## Footnote
Ventilation strategies include low PEEP and long expiratory times.
84
What is ECMO and when is it used in MAS?
Extracorporeal Membrane Oxygenation; used in infants with an oxygenation index (OI) >40
## Footnote
ECMO can improve survival rates in severe cases.
85
What complications can arise from Meconium Aspiration Syndrome?
* Respiratory failure
* Pulmonary hypertension
* Air leaks
## Footnote
These complications can significantly impact the infant's health.
86
What is the prognosis for infants with MAS?
Mortality rates range from 2.5% in developed countries to 32% in developing regions
## Footnote
Most deaths are due to respiratory failure and complications from MAS.
87
What is the pathophysiology of Acute Respiratory Distress Syndrome (ARDS) in newborns?
Systemic injury leads to lung inflammation and injury, often associated with multiorgan failure
## Footnote
This can occur due to asphyxia, shock, or sepsis.
88
What are common differential diagnoses for ARDS?
* Pneumonia
* Meconium Aspiration Syndrome (MAS)
* Respiratory Distress Syndrome (RDS)
## Footnote
Accurate diagnosis is critical for effective management.
89
What are the management strategies for ARDS?
* Treat underlying cause
* Surfactant administration
* Ventilation strategies to improve oxygenation
## Footnote
Fluid management is also essential to prevent lung flooding.
90
What is the primary treatment for the underlying cause of ARDS?
Treatment of the underlying cause of the ARDS
## Footnote
This includes various supportive and medical therapies.
91
How can surfactant administration affect ARDS?
Can improve oxygenation in ARDS, similar to MAS, but may require larger doses than used in RDS
## Footnote
Surfactant therapy is crucial in managing respiratory distress syndromes.
92
What are the key components of the ventilation strategy for ARDS?
* Increase FRC and improve oxygenation
* Increase mean airway pressure
* Higher PEEP
* Longer inspiratory time
93
What is the aim of fluid management in ARDS?
Decrease flooding of the lung with fluid restriction, while still maintaining proper perfusion of other organs
94
What is the recommended antibiotic regimen when systemic infection is suspected after 3 days?
Broad-spectrum antimicrobials, usually ampicillin plus an aminoglycoside
95
What are some complications associated with ARDS?
* Air leaks and infection
* Pulmonary hypertension
96
What might benefit pulmonary hypertension in ARDS patients?
Sedation or inhaled NO therapy
97
What is the mortality and morbidity rate of ARDS attributed to?
A combination of hypoxia from lung disease and effects of the systemic disease that caused the ARDS
98
When does early-onset pneumonia typically present?
Within the first 48 hours to 1 week after birth
99
What is the differential diagnosis for early-onset pneumonia?
* RDS
* TTN
* MAS
100
What organisms can cause transplacentally acquired pneumonia?
* Listeria monocytogenes
* Mycobacterium tuberculosis
* Treponema pallidum
* Rubella virus
* Cytomegalovirus (CMV)
* Herpes simplex virus (HSV)
* Adenovirus
* Influenza type A virus
101
What is the most common cause of early-onset pneumonia due to ascending infection?
Streptococcus agalactiae (GBS)
102
What percentage of women are colonized with GBS in developed countries?
20%–30%
103
What is the risk of invasive GBS disease in infants born vaginally?
1%
104
What is recommended for antenatal testing regarding GBS?
Recommended for all pregnant women
105
What has antenatal GBS prophylaxis achieved?
Decreased rates of early onset GBS sepsis and pneumonia but has not changed rates of late-onset disease
106
What is the second most common cause of early-onset neonatal sepsis and pneumonia?
E. coli
107
What are some other organisms that cause ascending infection?
* Haemophilus influenzae
* Streptococcus pneumoniae
* L. monocytogenes
* Klebsiella pneumoniae
* Candida albicans
* Adenovirus
* CMV
* HSV
* Echovirus
108
What are risk factors for early-onset pneumonia?
* Prolonged rupture of membranes
* Premature labor
* Colonization of the vagina with GBS or other pathogens
* Chorioamnionitis
109
How quickly can GBS infections present after birth?
Most present in the first 12 hours
110
What are some signs of pneumonia or sepsis in infants?
* Progressive tachypnea
* Respiratory distress
* Hypoxia
* Poor feeding
* Irritability
* Hypothermia
* Fever
111
What is a poor prognosis indicator in pneumonia cases?
* Overtly septic
* Poor peripheral perfusion
* Cyanosis
* Inadequate respiration
112
What is the radiographic finding in pneumonia?
Variable; can range from an entire lobe to segmental consolidation, atelectasis, or diffuse opacification
113
What is the importance of blood cultures in suspected pneumonia cases?
Important because many infections are hematogenously spread or have secondary bacterial release into the bloodstream
114
What is the initial treatment for early-onset pneumonia?
Ampicillin or benzylpenicillin and an aminoglycoside, most often gentamicin
115
What can be substituted for gentamicin in infants with birth asphyxia?
Cefotaxime
116
What is often required for H. influenza infections due to antibiotic resistance?
Cefotaxime
117
What is the treatment duration for most early-onset cases of pneumonia?
7–10 days
118
What are some complications that may arise from pneumonia?
* Lung abscesses
* Empyemas
119
What is the typical cause of late-onset pneumonia?
Most common causes are gram-positive cocci and gram-negative bacilli.
120
What are risk factors for late-onset pneumonia?
* Prolonged mechanical ventilation
121
What is the recommended treatment for Chlamydia trachomatis pneumonia?
2 weeks of oral erythromycin
122
What is a common cause of pneumonia in very low birth weight infants?
Fungal pneumonias, often due to Candida species
123
What is the recommended initial treatment for late-onset pneumonia if the infant is worsening?
Broadened to cover nosocomial organisms such as Pseudomonas and Serratia
124
What may aspiration pneumonia lead to?
Inflammation of the airways or physical obstruction of the airways
125
What can chronic microaspirations lead to in infants?
Hypoxia and respiratory distress
126
What is the management strategy for severe aspiration pneumonia?
Mechanical ventilation until inflammation has resolved
127
What should be considered in the differential diagnosis for term newborns with severe respiratory distress?
Childhood interstitial lung disease (chILD)
128
What conditions are included in chILD?
* Surfactant system problems
* Pulmonary interstitial glycogenosis (PIG)
* Neuroendocrine cell hyperplasia of infancy (NEHI)
* Alveolar capillary dysplasia (ACD)
129
What imaging is used to diagnose interstitial lung disease?
High-resolution computed tomography (HRCT) scan
130
What treatment is commonly used in many chILD cases?
Corticosteroids
131
What is persistent pulmonary hypertension of the newborn caused by?
Failure of the pulmonary vascular resistance (PVR) to rapidly decrease at birth
132
What happens to PVR during fetal circulation?
PVR is high and only 10%–20% of cardiac output goes through the pulmonary vasculature
133
What leads to rapid transitions from fetal to newborn circulations?
* Increased arterial oxygen content
* Removal of the low resistance of the placenta
* Removal of placental-derived prostaglandins
134
What causes pulmonary vascular pressure to decrease in newborns?
Aeration of the lungs which vasodilates the pulmonary vascular bed
135
What can chronic hypoxia and placental insufficiency lead to?
Intrauterine growth restriction infants with increased muscularization of pulmonary arterioles
136
What are some systemic conditions that can lead to pulmonary hypertension?
* Birth asphyxia
* Sepsis
* Metabolic disorders
* Maternal exposure to selective serotonin reuptake inhibitors
* BPD
137
What is the typical presentation of infants with pulmonary hypertension?
Usually present within 6 hours of birth with cyanosis and mild respiratory distress
138
What may indicate increased pulmonary pressures in PPHN?
A louder second heart sound and a soft systolic murmur from tricuspid regurgitation
139
What is the typical clinical presentation of pulmonary hypertension in newborns?
Usually presents within 6 hours of birth with cyanosis and mild respiratory distress
## Footnote
Grunting and nasal flaring are uncommon due to fully expanded lungs in PPHN.
140
What findings may indicate increased pulmonary pressures in newborns with pulmonary hypertension?
2nd heart sound may be louder and soft systolic murmur from tricuspid regurgitation (TR)
## Footnote
This is due to the increased pulmonary pressures.
141
What is a key diagnostic indicator for pulmonary hypertension when hypoxemia severity does not match clinical symptoms?
Suspected when the severity of hypoxemia does not correspond to the severity of radiologic or clinical symptoms.
142
What diagnostic tool is primarily used to diagnose pulmonary hypertension?
Echocardiogram
## Footnote
Necessary to rule out structural heart disease.
143
What is the most accurate echocardiographic predictor of pulmonary hypertension in children?
TR jet velocity.
144
What are some echocardiographic findings in persistent pulmonary hypertension of the newborn (PPHN)?
* RA enlargement
* RV dilation
* PA dilation
* Septal flattening
* Directional shunting at PFO or PDA.
145
What is the only way to directly measure pulmonary arterial pressures?
Cardiac catheterization.
146
What can be measured by the oxygen index or alveolar-arterial oxygen difference?
Severity of pulmonary hypertension and response to therapies.
147
What should be suspected in infants with severe pulmonary hypertension unresponsive to conventional therapies?
Alveolar capillary dysplasia (ACD).
148
What is a critical aspect of management for infants with pulmonary hypertension?
Minimal handling by staff and family.
149
What environmental condition is important for optimizing oxygenation in pulmonary hypertension management?
Normothermic environment.
150
What should be maintained within a normal range to optimize oxygen delivery in infants with pulmonary hypertension?
Hct (40%–50%).
151
What are two basic therapies for pulmonary hypertension?
* Optimize lung expansion
* Oxygen therapy.
152
What are the recommended pCO2 levels in the management of pulmonary hypertension?
Maintain pCO2 at 45 to 60 mmHg and pH > 7.25.
153
What should be avoided in terms of SpO2 levels in managing pulmonary hypertension?
Avoid SpO2 levels < 85 or > 97%.
154
True or False: Hyperventilation is routinely recommended as a therapy for PPHN.
False.
155
What is ECMO used for in the context of pulmonary hypertension?
Rescue therapy for infants unresponsive to other therapies.
156
What is the effect of low oxygen tension on pulmonary vasculature?
Causes vasoconstriction.
157
What is the only FDA-approved gas for treatment of pulmonary hypertension in term and late preterm infants?
Nitric Oxide (iNO).
158
What is a significant risk associated with the use of iNO?
Increased bleeding time and possible effects on surfactant function.
159
What is the recommended starting dose of iNO for treating PPHN?
10–20 parts per million (ppm).
160
What does PGI2 do in the context of pulmonary hypertension?
Modulates vascular muscle contraction by increasing cyclic-adenosine monophosphate to cause relaxation.
161
What is the role of sildenafil in the treatment of pulmonary hypertension?
Adjuvant therapy to iNO that inhibits the breakdown of cGMP.
162
What is a significant risk factor for pneumothorax in newborns?
Elective C-section increases the risk.
163
What is the typical presentation of a tension pneumothorax?
Contralateral shift of the central structures of the chest, severe desaturations, signs of shock.
164
What is the management for asymptomatic pneumothoraces?
Do not require treatment; will reabsorb over time.
165
What is a common presentation of pneumomediastinum?
Most are asymptomatic and do not require treatment.
166
What is the pathophysiology of pulmonary interstitial emphysema (PIE)?
Collection of air that escapes the alveoli and tracks along the sheaths of the small blood vessels of the lung.
167
What does chest radiograph typically show in cases of PIE?
Hyperinflation and diffuse, multiple, or small nonconfluent cystic radiolucencies.
168
What is the prognosis for pneumopericardium in infants?
High mortality and long-term morbidity.
169
What is the primary consequence of pulmonary interstitial emphysema (PIE)?
Decreased pulmonary perfusion and airway obstruction
## Footnote
Leads to increased lung compliance and areas of hyperinflation.
170
What is a common presentation of infants with severe PIE?
Profound hypoxemia and hypercarbia
## Footnote
This occurs upon presentation.
171
How is PIE typically diagnosed?
Chest radiograph (CXR)
## Footnote
Shows hyperinflation and cystic radiolucencies.
172
What does bilateral, diffuse PIE on a chest radiograph indicate?
Narrow cardiac silhouette due to mediastinal compression
173
What may form as air collects in the lung parenchyma in PIE?
Large bullae or pneumatoceles
## Footnote
Visible as circular air collections on the chest radiograph.
174
What is one management strategy for localized PIE?
Positioning the infant with the affected side down
## Footnote
May cause partial collapse of the lung and improve PIE.
175
What is the incidence of secondary pulmonary hypoplasia?
9 to 11 per 10,000 live births
176
What are the four main categories of etiologies for secondary pulmonary hypoplasia?
* Space-occupying lesions
* Chest wall deformities
* Severe oligohydramnios
* Disorders impacting lung development
177
What stage of lung development occurs between 6–17 weeks of gestation?
Pseudoglandular stage
178
What can limit lung growth during fetal development?
Lack of intrathoracic space and limitation in fetal breathing movements
179
What are common clinical features of secondary pulmonary hypoplasia?
Signs range from tachypnea to severe hypoxemic respiratory failure
180
What diagnostic tools can be used for pulmonary hypoplasia?
* Ultrasound (UTZ)
* MRI
* Chest radiography
181
What ratio indicates probable pulmonary hypoplasia?
Lung weight to body weight ratio <0.012
182
What management strategies are suggested for pulmonary hypoplasia?
* Low-pressure fast-rate ventilation
* Use of pulmonary vasodilators for pulmonary hypertension
183
What is a potential preventive measure for pulmonary hypoplasia?
Early detection and intervention of underlying causes during the antenatal period
184
What is the prognosis for pulmonary hypoplasia associated with severe oligohydramnios?
Estimated mortality of >90%
185
What is the incidence of patent ductus arteriosus (PDA) in term infants?
<0.1%
186
What causes patent ductus arteriosus (PDA)?
Failure of the ductus arteriosus to close after birth
187
What is the gold standard for diagnosing PDA?
Echocardiography
188
What management strategies are used for PDA in preterm infants?
* Fluid restriction
* Diuretics
* Cyclo-oxygenase inhibitors
189
What are common side effects of NSAIDs used for PDA treatment?
* Increased serum creatinine
* Hyponatremia
* Risk of gastrointestinal perforation
190
What is the prognosis of pulmonary edema in neonates?
Depends on the severity of the underlying condition
191
What are common etiologies associated with neonatal pulmonary edema?
* TTN
* Perinatal asphyxia
* Left ventricular failure
* RDS
192
What is a key feature of pulmonary hemorrhage in neonates?
Appearance of frank blood from the airway
193
What is the incidence of pulmonary hemorrhage in preterm infants?
Increased from 0.1% to 5.9% in the surfactant era
194
What are common risk factors for pulmonary hemorrhage?
* Hemodynamically significant PDA
* Acute left ventricular failure
* Surfactant administration
195
What are examples of upper airway obstruction causes?
* Choanal atresia
* Pierre-Robin syndrome
* Down syndrome
* Laryngomalacia
196
What is the incidence of upper airway obstruction?
The incidence is unknown
## Footnote
This highlights the difficulty in quantifying the occurrence of upper airway obstruction.
197
What are some examples of nasal-level upper airway obstruction?
Examples include:
* Choanal atresia
* Basal encephalocele
## Footnote
Choanal atresia is the most common congenital cause of nasal obstruction.
198
What syndrome can choanal atresia be part of?
CHARGE syndrome
## Footnote
CHARGE stands for Coloboma of the iris and retina, Heart disease, Atresia choanae, Retarded growth, Genital hypoplasia, Ear defects.
199
What craniofacial anomalies are associated with pharyngeal-level airway obstruction?
Craniofacial anomalies include:
* Macroglossia
* Retrognathia
* Micrognathia
200
What are the structural causes of laryngeal-level airway obstruction?
Structural causes include:
* Laryngeal polyps
* Cysts
* Laryngomalacia
## Footnote
Laryngomalacia involves collapse of epiglottis and aryepiglottic folds.
201
What percentage of cases of laryngeal obstruction is associated with injury to the recurrent laryngeal nerve?
20%
## Footnote
This injury is often caused by traction to the neck during delivery.
202
What are the clinical features of complete upper airway obstruction?
Features include:
* Persistent cyanosis
* Ineffective respirations
* Rapid deterioration if untreated
203
What is the typical presentation of unilateral choanal atresia?
May not exhibit clinical signs unless the unaffected side is blocked, leading to respiratory distress
204
How does bilateral choanal atresia present in infants?
Respiratory distress at rest, absent when crying or mouth breathing
205
What imaging techniques are used to diagnose upper airway obstruction?
Imaging techniques include:
* CT
* MRI
* Laryngoscopy
* Bronchoscopy
206
What is the management for nasal causes of upper airway obstruction?
Management includes:
* Oropharyngeal airway
* Surgical intervention for choanal atresia
207
What is the prognosis for mild forms of upper airway obstruction like laryngomalacia?
Often mild and resolves without specific intervention
208
What is the correlation between gastroesophageal reflux (GER) and respiratory issues in preterm infants?
The correlation is small
## Footnote
However, GER can lead to recurrent aspiration pneumonia.
209
What medications are commonly used to manage gastroesophageal reflux?
Medications include:
* Gastric acid suppressors
* H2 blockers
* Proton pump inhibitors
210
What risk is associated with the use of acid-blocking agents in preterm infants?
Increased risk of necrotizing enterocolitis (NEC) and sepsis, especially with gram-negative bacteria
211
What is Nissen fundoplication used for?
Used in some infants with severe gastroesophageal reflux
212
Fill in the blank: The most common congenital cause of nasal obstruction is _______.
Choanal atresia
213
True or False: Laryngomalacia usually resolves by the age of 18–24 months.
True
