Pediatric Pulmonology Flashcards
Infant respiratory distress syndrome
Formerly known as Hyaline
Membrane Disease
○ Most common cause of respiratory
distress in the preterm infant
○ More likely if born before 37 weeks
gestation
Cause of IRDS:
- Prematurity of the lungs
- Deficiency in pulmonary
surfactant
Surfactant
- Mixture of phospholipids & proteins synthesized & excreted
by Alveolar type II cells of the alveolus. - Decreases surface tension of the alveolar sac.
What cells make surfactant?
Alveolar type II
Surfactant deficiency =
high surface tension, alveolar collapse (atelectasis)
= ↑ pulmonary dead space
* Inflammation, pulmonary edema, hypoxia, poor oxygenation,
↑ respiratory effort, & eventually respiratory failure
Lung Development
- Surfactant production begins ~20 weeks
- ~24 weeks alveolar sacs are present (survival possible)
- Overall survival rate ~50%
- ~30% survive without severe morbidity
Best prevention of IRDS
Prevention of preterm birth
Alveoli collapse causes:
- Decreased gas exchange
- Decreased lung compliance &
functional residual capacity
Decreased gas exchange leads to:
○ Acidosis (Respiratory & metabolic)
○ Pulmonary vasoconstriction
○ Endothelial & epithelial breakdown
○ Leads to protein rich exudate
○ Hyaline membranes (accumulation of dead
cells and proteins that line the alveoli)
Decreased lung compliance &
functional residual capacity
○ ↑ dead space
○ V/Q (ventilation/perfusion)
mismatch & Hypoventilation
○ Right-to-left Cardiac shunt
○ Hypoxemia & hypercarbia
○ Respiratory acidosis
Clinical Presentation of IRDS
○ Respiratory distress (min.
to hours after birth)
○ Dyspnea
○ Retractions
○ Hypoxia
○ Grunting
○ Cyanosis
Diagnosis of IRDS
○ Chest X-ray
■ Diffuse signs of both interstitial
& alveolar congestion
■ Air bronchograms
■ Interstitial reticular pattern
■ “ground glass appearance”
○ ABG
o Blood cultures
Treatment of IRDS
○ Intratracheal surfactant administration
○ Supplementary oxygen as needed
○ Mechanical ventilation as needed
Intratracheal surfactant administration
○ Requires intubation
○ Best if followed by rapid extubation and switch to CPAP
○ Good evidence for CPAP immediately after delivery of premature
infant (keeps the alveoli open at the end of expiration)
○ Or MIST (minimally invasive surfactant therapy) just uses thin
catheter into the trachea.
What would glucocorticoids do in preventing IRDS?
○ Glucocorticoids administered to mother
○ Betamethasone or dexamethasone given to
mother if delivery necessary between 24-34
weeks
○ Stimulates maturation of the baby’s lung tissue & surfactant release
Exogenous Surfactant
○ Exogenous aerosol via endotracheal
tube
○ Used if pt unresponsive to CPAP or
HFNC
○ Natural & Synthetic Surfactant options
○ Natural may be superior
○ Poractant Alfa
○ Calfactant
○ Beractant
Complications of IRDS
● Respiratory Acidosis
● Metabolic Acidosis
● Pulmonary Edema
● Infection
● Air Leak - Pneumothorax,
Pneumomediastinum
● Necrotizing Enterocolitis
Bronchopulmonary Dysplasia
Formerly called Chronic Lung Disease of Infancy
● Chronic pulmonary condition
● Sequelae of neonatal acute respiratory
distress, regardless of cause
● Typically caused by prolonged
mechanical ventilation
Bronchopulmonary Dysplasia pathophysiology
○ Poorly understood
○ Supplemental O2 w/ premature
lungs
○ Barotrauma, Oxidative Stress
○ Premature lungs more
susceptible to inflammation
caused by mechanical
ventilation
“Considered present when there is prolonged need for
supplemental oxygen in premature infants after 28 days of
age… and who do not have other conditions requiring oxygen”
Bronchopulmonary dysplasia
Clinical Presentation of Bronchopulmonary Dysplasia
○ IRDS patients are at greatest
risk of developing BPD
○ Persistent respiratory
symptoms
○ Airway hyperreactivity
○ Requirement for continued
supplemental oxygen beyond
28 days old
Diagnostic Evaluation of Bronchopulmonary Dysplasia
Clinical diagnosis
○ Hx of prolonged ventilation
○ Need for continued O2
Assessing the patient several weeks
after birth helps determine severity
CXR will demonstrate non-specific findings
○ pulmonary edema, cystic spaces, atelectasis
Bronchopulmonary Dysplasia prevention
○ Therapeutic, but minimalistic approach to
mechanical ventilation preferred
○ Recognition of RDS & surfactant use
○ ↑ time on“vent” & ↑ O2 being delivered → ↑ risk of developing BPD
Bronchopulmonary Dysplasia treatment
- Nutrition supplementation (Many BPD
patients have oral hypersensitivity with
an aversion to eating) - Fluid restriction, diuretics
- O2 supplementation as needed
- Wean from mechanical ventilation and
O2 as quickly as possible - Exacerbations may require hospitalization
Prognosis of Bronchopulmonary Dysplasia
○ Ranges
● Lung function may be altered for life
○ Hyperinflation & damage to small
airways occasionally leads to COPD &
Pulmonary Hypertension later in life
○ Increased risk of developing asthma
Pediatric Pneumothorax
● Pneumothorax in children is uncommon,
but significant & life-threatening
● Highest risk = intubated, premature
neonates
Several causes of pediatric pneumothorax
○ Iatrogenic
○ Traumatic
○ Primary Spontaneous- without known lung disease
○ Secondary Spontaneous- with known lung disease
Pathophysiology of Pediatric Pneumothorax
○ Disruption of the pleural membrane (visceral or parietal)
→ loss of intrapleural negative pressure & lung collapse
● Hypoxia and dyspnea caused by
○ Decreased vital capacity
○ Decreased alveolar partial pressure
of O2
Pediatric pneumothorax Common signs & symptoms
■ Dyspnea
■ Cyanosis
■ Hypoxemia
■ Chest pain
○ Physical exam reveals ↓ breath sounds & hyperresonant percussion on the affected side
Diagnostic Evaluation of Pediatric Pneumothorax
○ Pneumothorax is generally a clinical diagnosis that can usually be confirmed with an upright Chest X-ray
○ A tension pneumothorax should be diagnosed based on clinical signs Death can occur before CXR is performed!
Pediatric Pneumothorax management and prognosis
○ If diagnosed in outpatient clinic setting, emergent transfer to the ER via EMS is advised.
■ Needle decompression immediately if tension pneumo
○ If large & symptomatic, chest tubes are placed to evacuate pleural space air & encourage lung re-expansion.
○ If the pneumothorax was an isolated event & treatment occurred quickly → good prognosis
○ If associated with trauma → prognosis is variable.
○ Risk of recurrence is high in Cystic Fibrosis patients.
Oxygen Therapy for Infants
● For a patient who is breathing spontaneously but is hypoxic, several
oxygen delivery methods are available.
● Different methods of delivery are
available, most common include the
Blow-by, Head hood, Nasal cannula, Face
mask, nCPAP, High Flow Nasal Cannula
(HFNC), Intubation
● Although the hood is efficient for young
infants, the nasal cannula is more often used
(more mobility).
● In contrast, head hoods & nonrebreather masks are able to
deliver concentrations as high as 90-100%.
● While providing oxygen therapy, pulse oximetry should be
monitored closely.
Even at high flow rates, O2 delivered by
nasal cannula rarely reaches inspired O2
concentrations over _____.
40-45%
T/F Too much oxygen therapy can be bad to the infant
T
Hyperoxia
may cause oxygen toxicity,
BPD, retinopathy of prematurity (ROP) (damage caused by oxygen free radicals)
Pediatric Sleep Apnea
● A condition characterized by partial or complete episodic airway
obstruction that occurs during sleep. (Snoring)
○ Usually accompanied by hypoxemia, hypercapnia, &/or sleep
disruption.
Risk factors of pediatric sleep apnea
○ Adenotonsillar hypertrophy
○ Obesity
○ Facial or laryngeal abnormalities
○ CNS dysfunction or disease
○ Neuromuscular disease
Pathophysiology of pediatric sleep apnea
○ One of the most common
causes in children is enlarged
tonsils & adenoids → upper
airway obstruction.
○ CNS disorders (like Cerebral Palsy or
brain stem compression) can cause a
central apnea.
○ Obesity of the face & neck can also
cause obstruction.
Clinical Presentation of pediatric sleep apnea
○ Snoring with apneic events & gasps.
○ Daytime (and nighttime) mouth breathing
■ Possible clue to tonsillar/adenoid hypertrophy or decreased
muscle tone of lips, tongue, and throat
○ Daytime sleepiness is seen, but is less common in kids than adults
○ Behavior issues, ADHD, anxiety/depression
Untreated Sleep Apnea
○ Associated with cardiovascular
complications
○ Impaired growth, & Failure to Thrive
○ Learning Problems
○ Behavioral Problems
Diagnostic Evaluation pediatric sleep apnea
○ Screen for snoring during WCCs.
○ A soft tissue lateral face/neck film may
show hypertrophy - Related to airway
abnormalities. (Down Syndrome)
○ Polysomnography is diagnostic for
obstructive & central apnea.
Pediatric Sleep Apnea management
○ Tonsillectomy & Adenoidectomy are mainstays of treatment.
○ Weight management in obese children
is often beneficial as well.
○ Continuous Positive Airway Pressure (CPAP)
is needed for patients who fail surgical
therapy, or those who are not surgical
candidates (known central apnea).
Foreign Body Aspiration risk factors
● Most common culprits are small, round
foods, such as hot dogs, grapes, berries,
nuts, seeds, etc.
● If the obstruction is significant,
progressive cyanosis, loss of
consciousness, seizures, bradycardia, &
cardiopulmonary arrest can follow
without treatment.
frequent cause of accidental pediatric death
Foreign Body Aspiration
Some common areas of foreign body lodging include:
○ Supraglottic airway- Most common
■ May trigger laryngospasm
○ Esophagus
■ Can compress the airway
○ Trachea
■ If object makes it through larynx
○ Large Bronchi
- Distal right bronchus is the most
common bronchial location
Most common area a foreign body will lodge if aspirated
Supraglottic airway
Treating a complete obstruction of FBA
○ If the patient is awake but unable to speak, moves air poorly, or is cyanotic, they are considered unstable & intervention is required immediately.
○ If under 1 year old, child should be placed face down over arm or lap.
Give 5 rapid back blows between the scapula, turn infant over & give 5
rapid chest compressions.
○ If over 1 year old, abdominal thrusts from behind (Heimlich maneuver)
should be attempted.
○ After back, chest, or abdominal thrusts, open mouth with jaw thrust &
carefully remove object if visualized. No blind sweeps!
Rigid Bronchoscopy is the gold standard for diagnosis for
Foreign Body Aspiration
Treating a partial obstruction
○ If patient is stable (forcefully
coughing & well oxygenated),
they may be able to forcefully
cough the object out.
○ If blockage progresses or patient’s
efforts fail, foreign body must be
removed with bronchoscopy or
laryngoscopy.
Treating a complete obstruction
○ If the child is unresponsive (or becomes unresponsive during back, chest, or abdominal thrusts), must start CPR, which may dislodge the object.
○ If complete airway blockage &
ventilation w/ bag-valve mask or
endotracheal tube fails, the skilled
clinician should consider a
Percutaneous Needle Cricothyrotomy.
Percutaneous Needle Cricothyrotomy
Performed by extending the neck,
attaching a 3-5 mL syringe to a 14-18
gauge IV catheter, & inserting catheter
through the cricothyroid membrane.
● Aspirate air to confirm position.
● Remove the syringe & needle, attach to ET
tube adapter & ventilate.
