Peds respiratory disorders Flashcards
Neonatal Respiratory Distress Syndrome (RSD)
general
Also known as hyaline membrane disease
Condition caused by structural and functional immaturity of the lungs
Undeveloped parenchyma
Inadequate production of pulmonary surfactant (Type II pneumocytes)
Most common cause of respiratory distress in preterm infants
Frequent cause of morbidity and mortality in neonates
Neonatal Respiratory Distress Syndrome (RSD)
Epidemiology
Risk is inversely related togestational ageat delivery
Highestincidencein babies born < 28 weeks of gestation
Higherincidencein white male infants
RSD
etiology(3)
prematurity and surfactant
Conditions that cause fetalacidosis (may ↓surfactantsynthesisand/or activity)
Genetic mutations affecting production of surfactant proteins
Prematurity
Lack of mature type II alveolar cells → insufficientsurfactantproduction
Different lipid and protein composition ofsurfactantin an immature lung → less activesurfactant
Surfactantinactivation
Meconiumor blood inalveoli(more common in term infants)
Oxidative and mechanical stress such as from mechanicalventilation
RSD
maternal and C section
Maternal diabetes
Maternal hyperglycemia→ fetalhyperinsulinemia
↑Insulinantagonizes the action ofcortisol, delaying lungsurfactantproduction
Cesarean delivery(CD) without labor
In the absence of labor,cortisolproduction (as well as other hormonal factors) is decreased
Altered fluid clearance from the fetal lung compared with vaginal delivery
Normal Fetal Lungs
Surfactant surge
Fetallungs
Not functional forgas exchange, and are filled with fluid (amniotic fluid)
Theplacentaserves as the fetus’s respiratory organ
Surfactant
Lipid-dense secretion (~80% phospholipids)
Produced in fetal development to prepare for air-breathing at birth
Appears in amniotic fluid between 28-32 weeks gestation
Surge in surfactant levels after 36 weeks
Reducessurface tensionwithin thealveoli
Prevents alveolar collapse at the end of theexpiration
↓ Risk ofatelectasisand ventilatory-perfusion (V/Q) mismatch in thealveoli
Respiration at Birth and RDS
Premature Lungs
Surfactant deficiency causing ↑ surface tension
↑ pressure is required for alveolar expansion
Lung instability at end-expiration
Low lung volume and ↓compliance
Collapse of portions of thelungs(atelectasis) → V/Q mismatch
RDS
Clin man
S/Sx and on auscultation
Respiratory distress
Starts within minutes or hours after birth
Becomes progressively worse over the first 48–72 hours of life
Tachypnea
Nasal flaring
Retractions
Expiratorygrunting
Cyanosis(from right-to-left shunting)
On auscultation:
Breath sounds may be normal or diminished, with a harsh tubularquality
Bilateral fine basal crackles
RDS
Cxray
ChestX-ray
Low lung volume
Bilateral, diffuse ground-glass appearance
Air bronchograms
Gas-filled bronchi surrounded by alveoli filled with fluid
Arterial blood gas(ABG)
Hypoxemia – improves with O2
Hypercapnia as disease progresses
Respiratoryacidosis
RDS
Management pre delivery
Prevention
Most effective preventive method is to avoid preterm delivery, when possible
Determine fetal lung maturity by amniocentesis
Usually performed after 32 weeks
Assess surfactant levels
Lecithin-to-sphingomyelin (L/S) ratio
Presence or absence of phosphatidylglycerol
RDS
management for preterm delivery and post delivery
If an early delivery cannot be avoided, treatment includes:
Antenatal corticosteroid therapy
Enhancessurfactantsynthesisandrelease
Accelerates lung maturity
Indicated for preterm delivery
Steroids are given 24-48 hours before delivery
Exogenoussurfactantreplacement therapy
Beneficial to preterm infants born < 30 weeks gestation
Provides support until endogenous production begins
Administration within 30–60 minutes of life provides the most benefit
Administered via endotracheal or less-invasive route (nebulization)
RDS
resusitation
Resuscitation
Airway, breathing, andcirculation (ABCs)
Respiratory support especially for babies under 28 weeksgestational age
The goal is for effectiveventilationand oxygenation in the least invasive manner possible
Nasal continuous positiveairwaypressure (nCPAP)
Endotrachealintubationand assisted mechanicalventilation for respiratory failure
Extracorporeal membrane oxygenation (ECMO)
Treatment that uses a pump to circulate blood through an artificial lung back into the bloodstream
Kussmaul breathing
increased depth of ventilation, but the rate is rapid (diabetic ketoacidosis)
Croup
general
Also known as laryngotracheobronchitis
Characterized by severe inflammation of the upper airway and most commonly caused by a viral infection
Primarily affects children aged 6–36 months
Potential affected age range: 6 months to 15 years
More prevalent in the fall and early winter
Transmission:
Aerosol droplets released by sneezing and coughing or by contact with infected secretions
Croup
Etiology
Etiology
Viral (75% of cases)
Most common: parainfluenza virus types 1 and 2
Second most common: respiratory syncytial virus (RSV)
Other causes: adenovirus, coronavirus, measles, influenza virus, rhinovirus, enterovirus, herpes simplex virus, metapneumovirus
Bacterial: usually present with high fever, look sicker than viral
Croup
Patho
Virus/bacteria infects the nasal and pharyngeal mucosal epithelium through aerosol droplets
Infection spreads to the larynx and trachea via respiratory epithelium
Infection triggers the infiltration of white blood cells
Edema ensues inside the trachea, larynx, and large bronchi
Edema partially obstructs the airway
Croup
S/Sx
Nasal discharge
Congestion
Coryza
Spasmodic, barking cough (common at night)
Inspiratory stridor – worsens with agitation
Fever
Hoarseness
Hoover’s sign (inward movement of the lower rib cage during inspiration)
Croup
Typical course (viral croup)
Initial symptoms:coryza, nasal congestion
12–48 hours:fever, barking cough, hoarseness,stridor
As disease progresses, respiratory distress (noted bytachypnea,dyspneaat rest, thoracic retractions, mental status changes) can occur
Disease lasts around 3–7 days (self-limited)
Croup
Dx
Clinical based on the presence of a“seal-like” barking cough and inspiratory stridor
for severe pts
Imaging
AP and lateral neck x-ray
Rule out other causes
Assess the severity of croup
AP neck x-ray usually shows a “steeple sign” which represents subglottic narrowing
Pearls & Pitfalls
Epiglottitis, retropharyngeal abscess, and bacterial tracheitis cause a more toxic appearance than croup and are not associated with a barking cough
croup
Croup
Westley Croup Score
Designed to measure severity of croup
Can be useful in determining treatment efficacy and patient disposition
Assesses 5 factors
Scores range: 0-17 points
Croup
Tx
Antipyretics
Corticosteroids (high-dose dexamethasone)
Improvement in airway inflammation/symptoms in 6–8 hours
0.6 mg/kg IM, IV, or orally once
Racemic epinephrine given by nebulization (moderate and severe disease)
5 to 10 mg in 3 mL of saline every 2 hours
Observe 3–4 hours after initial treatment
Supplemental oxygen
Cough medicines with dextromethorphan or guaifenesin should be avoided
Antibiotics are only prescribed in cases of primary or secondary bacterial infection
croup
Requirements for Outpatient Management
Non-toxic appearance
3-4 hours since the last nebulized racemic epinephrine
Able to tolerate fluids
No stridor at rest
Normal pulse oximetry
Reliable parents with a good understanding of return precautions
Close follow-up for moderate or severe cases
Croup
prognosis
Self-limiting disease that usually resolves within 3-7 days (80% of cases)
Life-threatening illness, but rarely progresses to death
Mortality occurs in <1% of intubated patients
Out-of-hospital cardiac arrest may occur
croup
complications
Complications (uncommon)
Pneumonia
Secondary bacterial tracheitis (high fever, toxic appearance, mucopurulent exudates in the trachea)
Respiratory failure
Pneumothorax
Recurrent symptoms (5% of cases)
Acute bronchiolitis
general
Acute inflammation of the small airways (bronchioles) most often secondary to viral infections
Common cause of hospitalization in infants in the United States
Peak incidence between 2-6 months of age
Seasonal preference:fall and winter
Acute bronchiolitis
Etiology
Viral infection:
Respiratory syncytial virus (RSV) – 1/3 of cases
Rhinovirus
Less common:
Human metapneumovirus, Parainfluenza virus, Influenza virus, Adenovirus, Mycoplasma pneumoniae, Pertussis
acute bronchilitis
RF
Prematurity (born < 34 weeks)
< 12 weeks of age
Low birth weight (< 2.5 kg)
Immunodeficiency
Congenital heart disease
Cystic fibrosis
Not breastfed
secondhand smoke
acute bronchilitis
patho
Pathological changes occur within 24 hours of contact with a pathogen:
Virus enters epithelial cells of terminal bronchioles
Inoculation causes inflammation → edema, mucus secretion, and epithelium sloughing
Sloughing and edema → narrowing and obstruction of small airways
Narrowing results in atelectasis and symptoms appear
Alveoli can over-inflate and become trapped with air
look for kid with lots of secretion, runny nose like faucet
acute bronciolitis
Sx
Symptoms vary based on the severity of the disease:
Initial 1–3 days (upper respiratory tract symptoms):
Cough
Congestion
Rhinorrhea
Peaks on day 3–5 (lower respiratory tract symptoms):
Wheezing and diffuse crackles on lung exam
Fever
Shortness of breath
acute bronchiolitis
Sx severe cases
Severe cases:
Apnea in infants, especially during sleep
Tachypnea
Cyanosis
Nasal flaring
Grunting
Intercostal retraction
Hypoxia < 92% saturation
acute bronchiolitis
Dx
Based onclinicalsuspicion:
Characteristic lower respiratory tract symptoms
Patients < 2 years
Presenting during the fall and winter seasons
Routine testing is discouraged → no therapeutic value
Further investigation:
Indications: high fever, severe presentation, history of comorbidities
Evaluate comorbid conditions or superimposed infection:
Complete blood count (CBC): leukocytosis
CXR: hyperinflation with atelectasis
RSV testing
acute bronchiolitis
Tx mild/moderate cases
Mild-to-moderate cases
Upright positioning during sleeping and feeds
Use of cool-mist humidifier and antipyretic
Bulb suctioning of oral and nasal secretions
Maintain hydration and feeding
Follow-up if patient worsens
acute bronchiolitis
Severe tx
Severe (< 28 days old, apnea, lethargic)
Hospital admission
Humidified oxygen and nebulized hypertonic saline
Suctioning of secretions
IV hydration
No evidence to support use of albuterol, epinephrine, or corticosteroids
Complications - pneumonia and respiratory failure
RSV
general
RNA virus; paramyxovirus family
Transmission via droplets (coughing, sneezing, kissing, touching infected objects then touching mucus membranes)
Seasonal epidemiology
RSV seasonality was altered following the COVID-19 pandemic; it is unknown if or when RSV will return to normal seasonality
RSV
presentation
Presentation:
Usually mild, cold-like symptoms
Serious illness (infants and older adults)
Highest risk among:
Premature infants
Young children with congenital heart or chronic lung disease
Young children who are immunocompromised
Adults 65 and older with compromised immune systems
Adults 65 and older with underlying heart or lung disease
Diseases Caused by Respiratory Syncytial Virus (RSV)
Infants:
Acute bronchiolitis
Pneumonia
Acute otitis media
Respiratory failure
Immunocompromisedor elderly adults:
Pneumonia
Acute exacerbation of underlying chronic illness (COPD,asthma,congestive heart failure)
RSV
Dx
Rapid antigen tests
Most common test
Nasal washings or nasal swabs
Results available in ~30 minutes
RSV RT-PCR
Molecular test that detects the genetic material of the virus
More sensitive than antigen testing or viral culture
Viral culture
Declining use
Costly and more difficult to perform
Several days to obtain a results
not normally done, does not change tx
RSV
Tx
Prophylaxis
Self-limited
Supportive care
Passive prophylaxis- for high risk kids
Palivizumab
Indicated for high-risk infant
First dose just before the onset of RSV season
Subsequent doses given at 1-month intervals (total of 5 doses)
whooping cough
general
What age is affected
Potentially life-threatening highly contagious bacterial infection of the respiratory tract caused by Bordetella pertussis (gram-negative coccobacillus)
Endemic worldwide
Incidence in the United States is affected by:
Immunity waning in previously vaccinated adolescents and adults
Anti-vaccination movement
Common and most severe in infants < 1 year of age
Transmission
Airborne droplets (coughing, sneezing, or speaking) or direct contact with oral or nasal secretions of an infected individual
Often affects 100% of non-immune household contacts
whooping
RF
Individuals at risk for contracting pertussis and/or severe disease include:
Unvaccinated individuals
Infants (especially < 4 months)
Pregnant women
Patients with an immunodeficiency
Patients with an underlying respiratory condition (COPD)
Older adults (> 65 years of age)
Those caring for infants
whooping
patho
whooping
Catarrhal
Catarrhal – most infectious stage
Lasts 1–2 weeks
Presents with nonspecific symptoms of an upper respiratory tract infection:
Low-grade fevers
Coryza
Sneezing
Conjunctival injection
whoopin
proxysmal
Paroxysmal
Lasts 2–8 weeks
Presents with the characteristic intense coughing (≥5 rapidly consecutive forceful coughs) followed by an inspiratory “whooping” sound
Frequently occurs at night
Whooping occurs ,ore frequently in older children and toddlers
Infants (< 6 months of age) may present with periods of choking orapnea(inability of the respiratory muscles to produce strong coughing)
Viscid (sticky) mucus from the nares
Post-tussive vomiting, shortness of breath (dyspnea), and cyanosis
whooping
convalescent
Convalescent
Lasts 4 weeks on average, but may extend for months
Characterized by the progressive reduction of all symptoms
whooping
Dx and prevention
Strong suspicion from a complete history and physical examination
Possible contact with other “whooping cough” cases
Vaccination status
Vaccine does not provide full protection; pertussis needs to be considered even in vaccinated children!
Laboratory confirmation is required
Nasopharyngeal swab → culture (gold standard) or PCR testing
Only reliable during the first 2-3 weeks of the infection
Serology testing
Can be used up to several weeks (2-8 weeks) after the onset of symptoms
A 2-fold rise in the antibody titer against pertussis is diagnostic
whooping
Tx
Hospitalization
Supportive care
Suction to remove mucus from the throat
Azithro
Hospitalization with respiratory isolation:
Infants < 1
Hypoxia
Apnea
Respiratory distress
Superimposed pneumonia
Unable to hydrate orally
Oxygen administration may be required in severe cases
whooping
Drug Tx
Macrolide
Catarrhal stage → ameliorate the disease
Paroxysmal stage → reduce the spread of pertussis, but do not affect the clinical course
Azithromycin 10 mg/kg PO once daily x 5 days
First-line choice for infants < 1 month of age
Erythromycin 10 mg/kg PO every 6 hours x 14 days (maximum 2 g/day)
Clarithromycin 7.5 mg/kg PO twice daily x 7 days (maximum 1 g/day)
Macrolide allergy → trimethoprim-sulfamethoxazole for patients > 2 months
whooping
Postexposure Prophylaxis
Given to every household contacts within 21 days of the onset of cough in the positive patient, whether they have been vaccinated or not
Erythromycin 500 mg PO 4 times daily x 14 days
Erythromycin 10 mg/kg PO 4 times daily x 14 days
Alternative antibiotics:
Clarithromycin and Azithromycin
Azithromycinis preferred for infants < 1 month of age
