Respiratory distress in the newborn Flashcards
Case
General Data:
CC: respiratory distress
History of Present Illness
Born FT to a 35 year G4P3 (3003) mother at home assisted by a TBA,
apparently normal at birth but after 8 hours, noted to have rapid
breathing and chest indrawing.
(-) prenatal check-ups
(-) no maternal illnesses during pregnancy
(-) previous pregnancies delivered normally
Ancillary History
Family Medical History: (-) Family history of bronchial asthma or
malignancy, (+) family history of DM and hypertension, (+) sibling
with Down syndrome
PHYSICAL EXAMINATION
General Survey
Awake, grunting
Anthropometrics
Weight =2.7kgs, length =51 cm, HC = 41, CC=43, AC= 37
Vital signs
BP 80/50 HR125 bpm RR 63 bpm T 36.5C O2 sats (room air) =
100%
Skin
No rash, no jaundice
Head and Neck
AFSF, pink conjunctivae, anicteric sclerae, (-) nasal congestion, (-)
cervical lymphadenopathies
Chest and Lungs
unequal chest expansion, (+) use of accessory muscles,
Cardiac
Adynamic precordium, displaced point of maximal impulse,
normal rate and regular rhythm, no murmurs
Abdomen
Normoactive bowel sounds, (+) flat abdomen,(-) hepatomegaly,
intact Traube’s space
Extremities
Full and equal pulses, (-) edema/cyanosis/clubbing, CRT less than 2 sec
LABORATORY RESULT:
CBC
Date Normal
WBC 5 x109/L
RBC 3.1x109/L
Hgb 110 g/L
Hct 0.38%
MCV 85fL
MCH 25 pg
Platelets 350x109/L
Neut% 0.7
Lymph% 0.3
Mono% 0.0
Eo% 0.0
Baso% 0.0
Chest radiograph AP: stomach, NGT, small bowel contents in L
thoracic cavity
What is your primary working impression?
Primary Working Impression
Congenital diaphragmatic hernia
basis for diagnosis?
Basis for Diagnosis
(8) History
(+) respiratory distress
normal at term birth but after 8 hours, noted to have
rapid breathing and chest indrawing
(+)sibling with Down syndrome
(9) Physical Examination
Grunting
Increased chest wall diameter
tachypnea
(+) use of accessory muscles
(+) bowel sounds in the L chest
displaced point of maximal impulse
(+) flat abdomen
What are your differential diagnosis for this case?
- CCAM
Respiratory distress
Decreased breath sounds
on 1 side
Radiographic finding: Cystic
lesion
Pulmonary sequestration
Respiratory distress Dullness to percussion an d
decreased breath sounds
over lesion
Continuous/ pure systolic
murmur with radiation to
the back may be heard
USG demonstrate systemic
artery
TTN
Respiratory distress Radiographic finding:
prominent vascular findings,
fluid in intralobar fissures,
flat diaphragm, small
pleural effusion
Resolves
Neonatal pneumonia
Respiratory distress Radiographic finding:
infiltrates or effusion
Eventration
Respiratory distress Caused only by elevation of
the entire hemidiaphragm,
with paradoxical motion of
affected diaphragm
No bowel sound on thoracic
cavity
What is your plan of management for this patient?
g. Diagnostic Tests/Labs
Chest xray
o CT scan, USG
CBC – Normal
h. Management
b.1. Goals of Management:
Pharmacologic Management
Pain control/ sedation
Non-pharmacologic management
Aggressive respiratory support
Intubation, avoid prolonged mask
ventilation which may further dilate the
bowel loops
Gentle ventilation with permissive
hypercapnia : MV or ECMO
Hydration
Request for echocardiography to guide
therapeutic decision by measuring
pulmonary and vascular pressures and
detect cardiac dysfunction
Surgical repair
b.2. Possible complications
Recurrence if patch used (patch does not grow
with patient)
PPHN
Bleeding, chylothorax, bowel obstruction
GERD
Neurocognitive defects
Anticipatory care
Proper nutrition
Vaccination
Mineral supplementation
What is respiratory distress syndrome?
- Hyaline Membrane Disease (HMD)
- RDS Type 1
- Syndrome in PT infants with RD due to inability to
generate the intrathoracic pressure necessary to
inflate the lungs without surfactant - PT ~50% of infants with BW 501-1500g
- Incidence is inversely proportional to the GA and BW
Etiopatho
- Deficiency or immaturity of surfactant, complicated by
overly compliant chest wall
- Effects of surfactant deficiency
o Inc surface tension causing alveolar collapse
o Progressive atelectasis, V/Q mismatch and
hypoxia
o Failure to develop an effective functional
residual capacity (FRC)
- Incidence is inversely proportional to GA (highest in
<28 wks AOG)
- RF: maternal DM, multiple births, CS, precipitous
delivery, asphyxia, and cold stress
- Surfactant – surface active material produced by type II
pneumocytes
o Synthesis begins at 24-28 weeks AOG,
appears in amniotic fluid at 28-32 weeks,
mature levels at 35 weeks AOG
§ Maturity delayed by fetal
hyperinsulinemia
§ Maturity enhanced by antenatal
CS and chronic intrauterine
stress
o Phospholipid (75%), protein (10%):
Dipalmitoylphosphatidylcholine
o Lipoprotein is released into the airways,
where it functions to decrease surface
tension and maintain alveolar expansion at
physiologic pressures
What are the clinical manifestations OF RDS
CM
Clinical course varies with the size of the infant, severity of
disease, use of surfactant replacement tx, presence of infection, degree of shunting of blood through the PDA, and whether or not assisted ventilation was initiated
1. RD soon after birth – tachypnea
2. prominent grunting – partial closure of the vocal cords
to prolong expiration and develop or maintain the FRC
à improves alveolar ventilation
3. intercostal/subcostal retraction – to develop high
transpulmonary P to reinflate the atelectatic air spaces
4. nasal flaring
5. cyanosis
6. N or dec BS, harsh tubular quality
7. Fine crackles on deep inspiration
8. Natural course is progressive worsening of cyanosis
and dyspnea
9. The CM reach a peak within 3d, followed by gradual
improvement
What are the diagnostics for RDS
Dx
1. CXR – characteristic “ground-glass” pattern or fine
reticular granularity of the parenchyma
- Low lung volumes and air bronchograms within the
first 24 h of life
- Uniform reticulogranular pattern and peripheral air
bronchograms
2. ABG – hypoxemia, hypercarbia, metabolic acidosis
3. Sepsis workup – CBC, BCS
4. 2D echo – r/o CV ds
5. Serum glu, E’ panel – r/o other causes of RD (hypogly,
hypoCa)
What is the management Hyaline Membrane Disease?
Mgt
1. Surfactant – dose 4ml/kg. recommended within 15 min
to infants <26 wks AOG, within 6h q6 for 2 doses
- For all PT with RDS who require delivery room
intubation for stabilization
- INSURE: Intubate-Surfactant-Extubate to CPAP
(intubate, administer surfactant intratracheally
through ET tube, connect to CPAP) reduces the need
for mechanical ventilation and development of
bronchopulmonary dysplasia (BPD)
- Reduces surface tension and stabilization of the
alveolar air-water interface
- SE: pulmonary hemorrhage, sec pulmonary infections,
air leak (pneumothorax) after bolus
- No longer cornerstone of tx
- Prophylactic surfactant only for:
o All <26 weeks AOG
o 26-28 wks requiring >30% FiO2
o >28 wks requiring >40% FiO2
2. CPAP – mainstay of tx for RDS (PEEP)
3. MV – only for severe RDS, respiratory failure,
persistent apnea
4. Fluid and nutritional support
5. Abx – for MC neonatal infections
How is this prevented?
Prevention
1. Prevent PT delivery
2. Antenatal CS –betamethasone 12mg q24h
- Dexamethasone 6mg IV q6 x4 doses: no longer
recommended due to cystic periventricular
leukomalacia
- For mothers at risk for PT delivery
3. Assessment of fetal lung maturity before delivery:
lecithin-sphingomyelin ratio and phosphatidylglycerol
- L/S ratio >2 = low risk of RDS
What is Transient tachypnea of the Newborn?
- “RDS type II”, “wet lung”
- Benign, self-limited RDS of FT and late PT infants
related to delayed clearance of lung fluid - MC perinatal respiratory disorder (40%)
What is the central mechanism of TTN?
delayed fluid resorption
What is the etiopathogenesis of RDS?
Etiopatho
- Central mechanism: delayed fluid resorption
o Inc lung compliance, inc airway resistance
- Lung fluid inhibits gas exchange, increased work of
breathing and compensatory tachypnea
- Hypoxia due to poorly ventilated alveoli
- RF:
o Cesarean section delivery – infant not
exposed to the stress (lack of catecholamine
surge and active Na reabsorption in the
lung) and in the absence of uterine
contractions (high transpulmonary P)
leading to lung fluid efflux
o M, macrosomia, prolonged labor, (-)
amniotic fluid phosphatidylglycerol, birth
asphyxia, fluid overload to the mother,
maternal asthma, delayed clamping of theumbilical cord (<45s), breech, fetal
polycythemia, infant of DM mom, infant of
drug dependent mom, VLBW, exposure to
B-mimetic agents
- At birth, the balance of fluid movt in the alveolus
switches from Cl secretion to Na absorption causing
resorption of intra-alveolar fluid
o Absorption occurs in 2 steps:
§ Na moves passively from the
alveolar lumen into the cell
through Na-K-ATPase pump
§ Na actively transported into the
interstitium by epithelial Na
channel (ENaC) à cleared by the
lymphatic and vascular system
what are the clinical manifestations of TTN?
CM
1. Early onset tachypnea – soon after birth or within the
1st 6 h after delivery
2. Retractions, nasal flaring, expiratory grunting, cyanosis
relieved by O2 supplementation
3. Barrel chest – due to AP diameter (hyperinflation)
4. Crackles
5. Palpable Liver and spleen – due to hyperinflation
6. Usually resolves within 48-72h
What are the diagnostics?
Dx
1. ABG – mild to mod hypoxemia, N partial CO2 due to
tachypnea
2. CXR – hyperinflation/ overaeration, prominent
perihilar streaking (engorged lymphatics)
- flattened diaphragm (lateral view)
- fluid in the intralobal fissures (rarely small pleural
effusion)
- prominent vascular markings: “fuzzy vessels” sunburst
pattern, peripheral air trapping
- mild/mod enlarged heart
3. Lung UTZ – double lung point: diagnostic
- Difference in echogenicity between UL and LL areas,
comet-tail artifacts
4. Sepsis workup – r/o infection
What is the management of TTN?
Mgt
1. Oxygenation and thermoregulation
2. Monitor fluid and e’
3. Salbutamol
4. Most resolve in 3-5d
5. Abx – while ruling out other ds entities
6. Feeding – dependent on RR:
a. <60: po
b. 60-80: OGT
c. >80: NPO, IVF
How is TTN prevented?
Prevention
1. Elective cesarean section scheduled at GA >39 wks
2. Vaginal birth
3. Establish fetal maturity prior to CS
4. Antenatal betamethasone prior to elective CS at term
What is meconium aspiration syndrome?
- With the passage of meconium in utero, the
meconium-stained amniotic fluid (MSAF) may be
aspirated. - MC in FT, postmature infants, and SGA
Etiopatho
- After in utero passage of meconium (fetal distress and
vagal stimulation), deep irregular respiration/gasping
can cause aspiration of MSAF
- Distal progression into the airways of MSAF occurs in
conjunction with reabsorption of lung fluid
- Early consequences include:
o Airway obstruction – Ball-valve effect:
meconium obstructing the small airways
causing atelectasis
o Chemical pneumonitis – due to release of
cytokines and vasoactive substances
o Release of inflammatory mediators
o Surfactant dysfunction
o Increase in pulmonary vascular resistance
and pulmonary hypertension: vasospasm,
hypertrophy of pulmonary musculature à
R-L shunting
- RF: postterm pregnancy, preeclampsia-eclampsia,
maternal HTN, mom DM, abN fetal HR, IUGR, abN BPP,
oligohydramnios, maternal heavy smoking, chronic CP
ds
What are the clinical manifestations of MAS?
CM
1. Mild to severe RD with cardiopulmonary failure
2. Early-onset RD in infant with MSAF
3. RD within the 1st hour: tachypnea, retractions,
grunting, cyanosis
4. Meconium staining of the skin – proportional to length
of meconium exposure and meconium concentrations
a. Stained umbilical cord: 15 min exposure to
thick MSAF or 1h to lightly MSAF
b. Yellow-stained nails: 4-6h
c. Stained vernix caseosa: 12h
5. Airway obstruction – RD, apnea, cyanosis, poor airexchange,
air-trapping, atelectasis, inc AP diameter of
the chest, air-leak syndromes, pneumomediastinum,
pneumothorax
6. Usually improves within 72h
What are the diagnostics?
Dx
1. ABG – hypoxemia, respiratory acidosis due to airway
obstruction/atelectasis/pneumonitis
- Combined respiratory and metabolic acidosis in
concomitant perinatal asphyxia
- Respiratory alkalosis: hyperventilation
2. CXR – hyperexpansion of the lungs with flat
diaphragms and widened rib spaces
- Widespread, coarse, asymmetric, patchy infiltrates
- Areas of lung atelectasis (complete obstruction)
flanked by irregular areas of overexpansion (partial
obstruction)
- Diffuse homogenous ground glass lung density
- Pneumothorax, pleural effusion, pneumomediastinum
3. Cardiac echo – pulmo HTN with resultant hypoxemia
from R-to-L atrial and ductal shunt
What is the management of MAS?
Mgt
1. ET intubation – only for depressed infants, with
suctioning to remove meconium in the airway before
the first breath
2. O2 – for RD and dec O2 sat
a. Mild ds: <40% for 48h
b. Mod: >40% for >48h
c. Severe: >48h (associated with PPHN)
3. MV – for moderate to severe MAS
4. Sedation – pain precipitates hypoxia and R-to-L
shunting
5. Abx – meconium inhibits the normally bacteriostatic
quality of the amniotic fluid, not routinely
recommended
6. ECMO – extracorporeal membrane oxygenation – final
rescue tx
