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)