Respiratory Problems Flashcards
Risk factors for RDS
- Male sex
- Maternal diabetes
- multiple birth (second twin esp)
- Elective caesarean
- Precipitous delivery
- Family history
- Sepsis
Protective factors for RDS
- Female sex
- PROM
- Antenatal steroids
- IUGR
- Chronic or gestational hypertension
- Maternal opiate or heroin use
What are the steps that occur in the normal transition to pulmonary respiration?
- Before birth - increased levels of catecholamines, vasopressin, prolactin and glucocorticoid enhance lung fluid resorption
- First breath triggered by decline in PaO2, acidosis and hypercapnia from interruption of placental circulation
- Air entry into lungs displaces fluid to establish FRC
- Increased pulmonary blood flow further enhances fluid resorption
Why do preterm infants have more difficulty in transition to pulmonary respiration?
- Surfactant deficiency increases surface tension and impairs ability to establish FRC
- Compliant chest wall means more energy required to generate sufficient negative pressure for first breath
3 types of apnoea and how do they differ?
- Obstructive apnoea - absence of airflow but persistent chest wall motion
- Central apnoea - no airflow or chest wall motion
- Mixed apnoea - most common in apnoea of prematurity - usually obstructive apnoea precedes central apnoea
What is the mechanism behind apnoea of prematurity?
Immature brainstem respiratory centres - attenuated response to CO2 and paradoxical response to hypoxia (causes apnoea rather than hyperventilation)
What is the mechanism of action of methylxanthines for apnoea of prematurity?
Increase respiratory drive by lowering threshold of response to hypercapnia, enhance contractility of diaphragm, prevent diaphragmatic fatigue
What are 5 types of lung injury that can be seen in RDS? (largely ventilator-induced)
- Atelectrauma - injury resulting from repeated alveolar collapse and expansion (recruitment/derecruitment injury)
- Volutrauma - overdistension of alveoli resulting from mechanical ventilation
- Barotrauma - pressure injury from ventilation
- Oxygen toxicity - caused by oxygen free radicals
- Ischaemic injury
What is the primary pathological change seen in respiratory distress syndrome?
Hyaline membranes in alveolar spaces.- formed from effusion of proteinaceous material from damaged cells and cellular debris
What cell type produces surfactant?
Type 2 pneumocytes
What is the composition of surfactant (and what component contributes to reduction in surface tension)?
- Phospholipids - lower surface tension
- Other lipids e.g. surfactant proteins A-D - facilitate adsorption and spreading of surfactant and have immunoregulatory properties
- Platelet activating factor
Typical radiological findings in RDS
Low lung volumes, ground glass appearance, air bronchograms
Below what gestation is routine antenatal corticosteroid administration recommended to reduce risk of RDS?
<37/40 (+consider before elective CS up to 38+6)
In relation to mechanical ventilation, what are the factors that affect oxygenation?
- FiO2
- Mean airway pressure (which depends on PIP, i-time, PEEP, RR [and thus e-time])
In relation to mechanical ventilation, what are the factors that affect ventilation/CO2 elimination?
Determined by minute ventilation - tidal volume (determined by PIP and i-time) and RR
Why is volume-targeted ventilation particularly important in RDS?
Rapid changes in lung compliance occur with surfactant treatment - high risk of volutrauma and air leak with pressure-limited ventilation. With VTV, PIP varies depending on respiratory compliance to achieve a set tidal volume
What are indications for high-frequency ventilation?
- Poor response to conventional ventilation
- Severe RDS
- Severe MAS
- Pulmonary interstitial emphysema (PIE)
- Recurrent pneumothorax
Risks of surfactant administration
- transient hypoxia, hypercapnia, bradycardia, hypotension
- ETT blockage
- Pulmonary haemorrhage
Definition of bronchopulmonary dysplasia
Requirement for supplemental oxygen for ≥ first 28 postnatal days
How is the severity of bronchopulmonary dysplasia classified?
Classified at 36/40 PMA
- Mild BPD = breathing RA at 36/40
- Moderate BPD = 22-29% O2 at 36/40
- Severe BPD = positive pressure support or >30% O2
What are proven strategies to reduce risk of BPD?
- Early use of nCPAP
- Early selective surfactant use
- Use of volume targeted ventilation
- Use of caffeine for apnoea of prematurity (load pre-extubation)
- Systemic corticosteroids (reduce mortality and BPD but increase risk of CP and neurodevelopmental disability)
Risk factors for TTN
- Late prematurity
- Twin gestation
- Maternal asthma
- Precipitous delivery
- Gestational diabetes, macrosomia
- Caesarian section without labour
What is the pathophysiology of TTN?
ineffective expression or activity of ENaC or Na/K-ATPase -> slowed absorption of fetal lung fluid -> reduced pulmonary compliance and impaired gas exchange
Risk factors for MAS
- Term or post-term (esp >42/40)
- SGA
- Perinatal asphyxia
What should be considered in the cause of in utero passage of meconium in a preterm infant (<34/40)
Congenital listeriosis
What are 5 mechanisms by which meconium aspiration can effect lung function?
- Airway obstruction (complete causing atelectasis and V/Q mismatch, or partial creating ball-valve effect and air trapping)
- Chemical pneumonitis
- Surfactant deficiency/inactivation (lipid content of meconium displaces surfactant, and can reduce synthesis)
- Increased risk of infection - sterile but is good growth medium for E.coli; passage of meconium may result from intrauterine infection
- PPHN - from hypoxaemia, hypercapnia, acidosis; chronic fetal hypoxia causes remodelling of pulmonary vasculature
Radiological features of MAS
- Patchy infiltrates
- Hyperinflation
- Areas of air trapping
- Homogenous opacification later from pneumonitis
Treatments for MAS
- Positive pressure ventilation - higher e-time to prevent air trapping
- Surfactant replacement (reduces need for ECMO)
- iNO for PPHN
- HFOV or ECMO for MAS refractory to conventional ventilation
Causes of pulmonary hypoplasia
- Reduced amniotic fluid production - Potter syndrome/sequence from renal agenesis, infantile ARPKD, posterior urethral valves etc
- Amniotic fluid loss - preterm rupture of membranes (only if ROM <26/40), amniocentesis w chronic leakage
- Lung compression - pulmonary space occupying lesions (CDH, CPAM, pleural effusion), thoracic abnormalities (thoracic dystrophies)
- Reduced fetal movements - neuromuscular disease, oligohydramnios
What is the most common type/location of congenital diaphragmatic hernia?
Bochdalek hernia (posterior portion of diaphragm) - 90% (80-90% on the left)
What other anomalies are associated with CDH?
- Pulmonary hypoplasia
- Intestinal malrotation (20%)
- Chromosomal abnormalities - T21, T13, T18, Fryn’s, Cornelia-de-lange, Turners
- Omphalocoele
- Esophageal atresia
- CNS lesions, cardiac lesions
Predictors of outcome in CDH
- Liver position in chest (poor prognosis)
- expected:observed lung ratio
- lung:head size ratio
Clinical signs of congenital diaphragmatic hernia
- Respiratory distress (may occur after ‘honeymoon period’ >48hrs as gut becomes more air filled)
- Scaphoid abdomen, incr chest wall diameter
- Reduced breath sounds (often bilateral)
- Bowel sounds in chest
- Mediastinal shift
Key principles in management of CDH
- Avoid mask PPV
- Early intubation for respiratory distress
- Widebore NG tube to decompress gut
- Gentle ventilation with permissive hypercapnia to reduce lung injury (may need HFOV or ECMO)
- Delayed surgical repair (at least 48hrs after stabilisation improves outcome)
Predictors of poor outcome for CDH
- Size of defect - strongest predictor
- Early onset of symptoms
- Associated major anomaly
- Severe pulmonary hypoplasia
- Herniation to contralateral lung
- Need for ECMO
Complications following CDH repair
- GORD
- Recurrence
- intestinal obstruction
- Poor growth
- Pectus excavatum
- Pulmonary problems/BPD
- Neurocognitive deficits
What is subcutaneous emphysema in a newborn nearly always indicate?
Pneumomediastinum
What type of patient does pulmonary interstitial emphysema usually effect?
VLBW infants with RDS (occurs in up to 25%)
Risk factors for pulmonary haemorrhage
- Acute pulmonary infection
- Severe asphyxia
- RDS
- Assisted ventilation
- PDA
- Bleeding diathesis (HDN, thrombocytopenia)
- Surfactant treatment
Treatments for acute pulmonary haemorrhage
- Blood replacement
- Intratracheal adrenaline
- Tamponading by increasing mean airway pressure
- Surfactant administration (intraalveolar blood can displace/inactivate surfactant)
