Resp Flashcards
What is RDS?
A respiratory disorder seen in newborn premature infants, due to surfactant deficiency
What is the aetiology of RDS?
Surfactant is a mixture of phospholipids and proteins excreted by type II pneumocytes of alveolar epithelium
- It lowers the surface tension of the lungs
- Most is produced after 30wks gestation (so deficiency is seen in preterm infants)
- Surfactant deficiency causes alveolar collapse on expiration → increases the energy required for breathing
- Development of interstitial oedema makes the lungs even less compliant → leads to hypoxia and retention of CO2
- Right-to-left shunting may occur though collapsed lung (intrapulmonary) or if pulmonary HTN is severe, across the ductus arteriosus and foramen ovale (extrapulmonary)
The more preterm the infant, the higher the incidence of RDS
- May rarely occur in term infants of diabetic mothers or from genetic mutations in the surfactant genes
What are the causes of secondary surfactant deficiency?
Secondary surfactant deficiency may occur due to:
- intrapartum asphyxia,
- pulmonary infection,
- pulmonary haemorrhage,
- meconium aspiration,
- oxygen toxicity,
- congenital diaphragmatic hernia
What are the RFs for RDS?
- prematurity,
- male,
- C-section without maternal labour,
- perinatal asphyxia,
- maternal DM,
- FHX of RDS
What is the epidemiology of RDS?
- RDS is very common in infants born <28wks gestation;
- 50% infants born at 28-32wks
What are the signs and symptoms of RDS?
- Signs of respiratory distress
- Begin at delivery or within 4-6hrs of birth, peak at 48-72hrs, then start to improve
- May rapidly progress to fatigue, apnoea and hypoxia
What are the signs and symptoms of respiratory distress?
A group of signs and symptoms that essentially mean the child/infant is SOB
- Signs of respiratory distress:
- Tachypnoea, tachycardia
- Laboured breathing, subcostal and intercostal recession, nasal flaring, tracheal tug
- Expiratory grunting (to create positive airway pressure during expiration and maintain FRC)
- Head retraction
- Inability to feed
- Severe: cyanosis, tiring, reduced consciousness, O2 sats <92% despite O2 therapy
What are the Ix in ?RDS?
-
Pulse oximetry
- Maintain O2 sats at 91-95%
-
Blood gases
- Respiratory acidosis (due to alveolar atelectasis and overdistension of terminal airways)
- Metabolic acidosis (due to lactic acidosis from poor tissue perfusion)
- Hypoxia (due to right-to-left shunting)
-
CXR
- Diffuse granular/ground glass appearance
- Monitor FBC, U&Es, LFTs, glucose
-
Echocardiogram
- Rule out PDA, determine direction and degree of shunting, make diagnosis of pulmonary HTN
- Blood cultures → to rule out sepsis
What is the antenatal Tx to prevent RDS?
- Antenatal corticosteroids if preterm delivery anticipated → stimulate surfactant production
- Significantly reduce RDS, bronchopulmonary dysplasia and IVH
- Tocolytics to delay preterm birth
- Neonatologist/NICU involvement for at-risk infants
What is the Mx of RDS?
- ABCDE approach
-
Give oxygen
- Oxygen therapy in preterm infants:
- Oxygen must be given to correct hypoxaemia, but excess is damaging (due to free radicals)
- Start with 21-30% oxygen; in term infants use air
- In preterm infants keep O2 sats 91-95%
- Oxygen therapy in preterm infants:
-
Surfactant therapy
- Given directly into the lungs via endotracheal tube or catheter
- Prophylactic intratracheal administration of surfactant to infants at risk of RDS
-
Additional respiratory support
- Non-invasive: CPAP, high-flow nasal cannula
- Preferred over mechanical ventilation fewer complications
- Invasive: mechanical ventilation via a tracheal tube
- With intermittent positive pressure ventilation (IPPV)
- Non-invasive: CPAP, high-flow nasal cannula
-
Supportive therapy
- See preterm infant management – temperature control, minimal handing, antibiotics etc.
What can happen in RDS if the O2 sats are too high (e.g. >95%)
Too high → retinopathy of prematurity, BPD
What can happen in RDS if the O2 sats are too low (e.g. >92%)
- Too low → necrotising enterocolitis, death
What are the complications of RDS?
-
Acute:
- Damage from ventilation e.g. CLD
-
Pneumothorax (10%)
- Overdistended alveoli → rupture → air tracks into interstitium → interstitial emphysema
- Reduced breath sounds/chest movement, transilluminates
- Prevent by ventilating with lowest possible pressures
- IVH (increased risk if mechanical ventilation)
- Persistent pulmonary HTN
- Necrotising enterocolitis
-
Chronic:
- Bronchopulmonary dysplasia
- Retinopathy of prematurity (esp if excess O2 used)
- Neurological impairment (related to prematurity and hypoxia
What is bronchopulmonary dysplasia?
- Chronic lung disease that affects premature infants,
- defined as infants who still have an oxygen requirement at corrected age of term (37wks gestational + chronological age)
- AKA chronic lung disease (CLD) of prematurity
What is the aetiology of bronchopulmonary dysplasia?
Usually seen in premature infants who have needed mechanical ventilation and oxygen therapy for RDS
- Sometimes occurs in premature infants with few signs of initial lung disease, or term infants who needed ventilation
What is the pathophysiology of bronchopulmonary dysplasia?
Pathology is multifactorial:
- Lung damage secondary to pressure (barotrauma) and volume (volutrauma) from artificial ventilation
-
Oxygen toxicity (>40% inspired oxygen is toxic to immature lung)
- Oxygen causes generation of superoxides, hydrogen peroxide and oxygen free radicals
- Activation of inflammatory mediators (secondary to free radicals, barotraumas and infection)
- Inadequate nutritional supplement, related RDS/lung disease
Histology shows interstitial oedema, mucosal metaplasia, interstitial fibrosis and overdistended alveoli
What is the epidemiology of bronchopulmonary dysplasia?
Affects 20% of ventilated newborns
Risk of developing BPD is inversely related to gestational age and BW
What are the signs and symptoms of bronchopulmonary dysplasia?
- Most common clinical scenario is a 23-26wk gestation baby who over 4-10wks progresses from needing ventilation to CPAP to supplemental O2
- Many babies continue to have signs of respiratory distress
-
Poor weight gain (if severe)
- Due to difficulties feeding and higher energy requirements
What are the Ix indicated in a picture of ?bronchopulmonary dysplasia?
-
Continuous pulse oximetry
- To establish oxygen requirements and ensure appropriate oxygenation
-
ABG
- Compensated respiratory acidosis reflecting chronic high pCO2, relative hypoxia
-
CXR
- To make diagnosis and assess complications
- Shows widespread areas of opacification, hyperinflation, sometimes with cystic changes
What is involved in the prevention of bronchopulmonary dysplasia?
- Prevention of RDS (antenatal corticosteroids, surfactant)
-
Appropriate and careful ventilation if needed;
- don’t over-oxygenate;
- early extubation to nasal CPAP
What is the Mx of bronchopulmonary dysplasia?
Respiratory support:
- ABCDE approach
- Mainstay of management
- Most babies are weaned onto CPAP or high-flow nasal cannula, followed by ambient oxygen (may take several months)
- Some babies need long-term artificial ventilation
-
~ corticosteroids given for earlier weaning from ventilator
- But neurodevelopmental risks → only given to those who are ‘stuck’ on the ventilator
Long-term management:
- Home oxygen may be needed
- Support by community children’s nurses, ‘Hospital at Home’ team
What are the risks of corticosteroids to a newborn neonate?
neurodevelopmental risks
What are the complications of bronchopulmonary dyplasia?
- Pulmonary hypertension
- Infection (esp pertussis, RSV pneumonia) may cause respiratory failure
- Poor neurodevelopmental outcome
What is persistent pulmonary HTN of the newborn?
Life-threatening condition caused by persistently raised pulmonary vascular resistance after birth
What is the aetiology of persistent pulmonary HTN of the newborn?
What is the epidemiology of persistent pulmonary HTN of the newborn?
0.5% live births
Usually occurs in term or late preterm infants
What are the signs and symptoms of persistent pulmonary HTN of the newborn?
- Usually presents in first 24hrs of life
- Signs of respiratory distress
- Cyanosis
- Signs of cardiogenic shock (due to myocardial ischaemia and papillary muscle dysfunction)
- Hypotension, oliguria, prolonged cap refill
What are the Ix for persistent pulmonary HTN of the newborn?
-
Pulse oximetry
- Hypoxia
- Out of proportion to parenchymal lung disease on CXR; doesn’t respond to 100% O2
- >10% difference between pre- and postductal (R thumb and either big toe)
- Due to R to L shunting through PDA (but not always present)
- Hypoxia
- ABG
-
CXR
- Usually normal, may show findings of an associated condition
-
Echocardiogram
- Urgent → diagnostic
- To exclude congenital heart disease, identify signs of pulmonary HTN (e.g. raised pulmonary pressures, tricuspid regurgitation), assess extent to shunting
What is the Mx for persistent pulmonary HTN of the newborn?
Ventilatory and circulatory support:
- ABCDE approach
- Give oxygen
- Mechanical ventilation (high-frequency) if needed
- ECMO (extracorporeal membrane oxygenation) if other treatments fail
- IV fluids, vasopressors (e.g. dopamine)
- Correct acidosis
Inhaled nitric oxide
- Potent vasodilator
- Sildenafil (Viagra) is another vasodilator which can sometimes be used
What are the complications of persistent pulmonary HTN of the newborn?
- HIE, CP, developmental delay etc.
- NEC
- ARF
What is the prognosis of persistent pulmonary HTN of the newborn?
Prognosis depends on underlying pathology; high morbidity and mortality
What is transient tachypnoea of the newborn?
A common, self-limiting tachypnoea in the absence of other causes
Aetiology of transient tachypnoea of the newborn?
Caused by delay in the reabsorption of foetal alveolar fluid
- The process of clearing foetal alveolar fluid begins before term birth and continues through labour/delivery
- In late gestation the mature lung epithelium switches from actively secreting liquid into the air spaces, to actively resorbing liquid (partly due to Na+ resorption)
- If there is short delivery or C-section (without labour), mechanisms to reabsorb alveolar fluid are not established
- Leads to pulmonary oedema, decreased pulmonary compliance, decreased tidal volume and increased dead space
Epidemiology of transient tachypnoea of the newborn?
Most common cause of respiratory distress in term infants (0.5%)
Signs & symptoms of transient tachypnoea of the newborn?
- Signs of respiratory distress
- Usually at the time of birth, within 2hrs of delivery
- Most prominent feature is tachypnoea (>60 in neonates); hypoxia and cyanosis are rare
Ix of transient tachypnoea of the newborn?
- Clinical diagnosis
-
CXR
- To support diagnosis
- Prominent perihilar streaking (distended pulmonary veins and lymphatics), patchy infiltrates, fluid in the horizontal fissure, flat diaphragms
-
Exclude other causes
- ABG (exclude metabolic acidosis, degree of decreased pO2 depends on amount of fluid in lungs)
- Blood cultures (exclude infection)
Mx of transient tachypnoea of the newborn?
Supportive management
- Respiratory support
- Additional ambient O2; may need nasal cannula, occasionally CPAP
- Maintain hydration, IV fluids
- NBM until RR <60 to decrease aspiration risk
- Prophylactic antibiotics (until negative blood cultures)
Complications and prognosis of transient tachypnoea of the newborn?
Benign and self-limiting; usually no complications
Usually settles within 1st day of life; can take several days to resolve completely
What is a congenital diaphragmatic hernia?
Congenital defect in the formation of the diaphragm, allowing protrusion of abdominal contents into the chest cavity
What are the 3 types of congenital diaphragmatic hernia?
There are 3 types:
-
Posterolateral Bochdalek’s hernia (main focus):
- Most common, usually L sided (85%); occurs at 6wks gestation
- L sided hernias allow herniation of small bowel, large bowel, and intra-abdominal solid organs
- R sided hernias allow herniation of liver and a portion of large bowel
- Leads to pulmonary hypoplasia, persistent pulmonary HTN of the newborn, L ventricular hypoplasia (if very severe)
-
Anterior Morgani’s hernia:
- 3%; small and easily repaired
-
Hiatus hernia:
- Stomach herniates through oesophageal hiatus à GORD
- Only needs repair if severe symptoms
RFs for congenital diaphragmatic hernia?
- previous affected sibling,
- cardiac abnormalities (25%),
- renal abnormalities
- Karyotype abnormalities are seen in 4% infants → associated with trisomy 13, 18, 21, Turner’s syndrome
Signs and symptoms of congenital diaphragmatic hernia?
Usually discovered on antenatal USS screening or following polyhydramnios in the mother
- If not detected antenatally, presents at or very soon after birth with:
- Signs of respiratory distress
- Absent breath sounds on one side of the chest, usually the L with heart shifted to R
- Bowel sounds audible over chest wall
- Smaller defects may present later with ‘wheezy child’ or recurrent chest infection
Ix for congenital diaphragmatic hernia?
- Antenatal USS
- Allows detailed planning of delivery and immediate care of the neonate
-
CXR
- Shows loops of bowel in the chest
- Confirms diagnosis if not previously diagnosed
-
Assess for other abnormalities:
- Echo
- Renal USS
- Karyotyping
Mx for congenital diaphragmatic hernia?
Immediate management:
- ABCDE approach
-
Endotracheal intubation and mechanical ventilation if severe; ECMO if necessary
- Avoid bag-and-mask ventilation in delivery room because stomach/intestines become distended with air à further impaired lung function
- NG tube passed and suction applied à decompression of stomach
- Consider surfactant
- Monitor blood gases, put indwelling venous catheter in to enable drug administration
- BP support with volume expansion/inotropic agents/colloid
Surgical management (after stabilisation):
- Abdo organs are replaced into abdo cavity and diaphragmatic defect is repaired
Complications and prognosis of congenital diaphragmatic hernia?
Complications:
- Pulmonary hypoplasia, persistent pulmonary HTN, surfactant deficiency → chronic lung disease
- Pneumothorax in normal lung (due to resuscitation)
- Intestinal malrotation, volvulus
- Neurodevelopmental delay (due to hypoxia)
Overall survival is 50%; high mortality if related to pulmonary hypoplasia
What is meconium aspiration?
Aspiration of meconium (the first faeces of a neonate) into the respiratory system
Meconium aspiration syndrome (MAS): spectrum, leading to various degrees of neonatal respiratory distress
What is the pathophysiology of meconium aspiration?
- Meconium is passed due to in-utero peristalsis
- Usually occurs when GI maturation is sufficient (i.e. in term babies)
- Also passed in response to foetal distress (hypoxia, head compression, cord compression, etc.)
- Foetal distress/hypoxia causes foetal gasping à meconium aspiration into the lungs (from meconium-stained amniotic fluid)
- May happen antenatally or perinatally
- In the lungs, meconium leads to:
- Mechanical airway obstruction (partial/total)
- Leads to decreased ventilation of small airways and air trapping à pneumothorax, increased pulmonary vascular pressure (à R to L shunt)
- Pulmonary inflammation (pneumonitis)
- Due to pro-inflammatory cytokines in meconium
- Surfactant dysfunction
- The inflammatory reaction deactivates surfactant à reduced gas exchange à exacerbates hypoxia
- Mechanical airway obstruction (partial/total)
- This leads to:
- Foetal hypoxia
- Infection
- Persistent pulmonary HTN (due to remodelling of pulmonary vasculature due to hypoxia)
RFs for meconium aspiration?
- gestational age >42wks,
- foetal distress,
- intrapartum hypoxia,
- Apgar score <7,
- chorioamnionitis,
- PROM,
- oligohydramnios,
- IUGR,
- maternal HTN/DM/pre-eclampsia/smoking/drug abuse
Risk is highest in infants who are post term and suffered birth asphyxia
Rare if <34wks gestation (GI tract not mature enough)
Epidemiology of meconium aspiration?
Meconium is passed by 10-20% babies; incidence increases with gestation (25% by 42wks)
Of the babies that pass meconium, 10% develop meconium aspiration syndrome
Signs and symptoms of meconium aspiration?
-
Antenatal/perinatal:
- Foetal distress on CTG
- Meconium-stained amniotic fluid
-
Signs of respiratory distress
- At birth or within 4hrs
-
Signs of post-maturity and meconium staining
- Yellow/green skin, long stained nails, dry/scaling skin
Ix for meconium aspiration?
- Pulse oximetry (dual)
- CXR
- Confirm diagnosis
- Patchy infiltrations, consolidation, pleural effusion, flattened diaphragms/increased lung volume
- Bloods:
- FBC, CRP, blood cultures (for infection)
- ABG: hypoxaemia, hypercarbia, metabolic acidosis
Mx for meconium aspiration?
Depends on severity; may need NICU
1.Supportive care:
- Place under infant warmer
- Oxygen therapy:
- Nasal canula, CPAP, mechanical ventilation
- Nutritional support (IV fluids, switch to NG/oral when possible)
2. Antibiotics:
- IV ampicillin + gentamycin
- If clinical suspicion of infection (e.g. chorioamnionitis, PROM, foetal heart-rate abnormalities)
- Can be stopped if 48hr cultures and clinical examination findings are negative
3. Surfactant:
- May be given in moderate MAS or if pneumothorax is present
4. Inhaled nitric oxide:
- If pulmonary hypertension is also present
Complications and prognosis of meconium aspiration?
Complications:
- Pneumothorax or pneumomediastinum (due to alveolar overdistention from obstruction)
- Persistent pulmonary hypertension of the newborn (1/3)
- Bronchopulmonary dysplasia
- Neurodevelopmental delay (due to hypoxia)
Prognosis depends on degree of hypoxia and complications
- 80% have a 3-4d illness and are then discharged
- 20% require NICU due to increased respiratory and cardiovascular requirements
What is the common cold?
Self-limiting inflammation of the upper respiratory tract mucosa that may involve nose, throat, sinuses and larynx
Coryza: acute inflammation of the mucous membranes of the upper respiratory tract (i.e. a cold; also caused by hay fever)
Coryzal symptoms: the symptoms seen in the common cold
Aetiology of the common cold?
Most common pathogen is rhinovirus (>100 different serotypes) – 50%
- Also caused by coronavirus (10-15%), influenza (5-15%), parainfluenza (5%), RSV (5%)
Infection leads to influx of polymorphonuclear leukocytes into the nasal submucosa à inflammation
Reinfection can occur after re-exposure to the same vial subtype (usually milder and of shorter duration)
RFs are exposure to infected people, winter
Epidemiology of the common cold?
The most common infection in childhood à children have 6-8/yr; adults have 2-4
Peaks when starting nursery and primary school
Signs and symptoms of the common cold?
- Onset over 1-2d
- Rhinorrhoea (clear or mucopurulent)
- Sneezing
- Nasal blockage
- Sore throat (red on examination)
- Cough (may persist for up to 4wks)
- Low-grade fever (variable)
- Lethargy, poor feeding
Ix for the common cold?
clinical diagnosis
Mx for the common cold?
Educate patients
- Colds are self-limiting and have no specific curative treatment; antibiotics do not work (viral infection)
- Hygiene measures to limit the spread to others
Symptomatic management
- Rest, maintain fluid intake
- Paracetamol or ibuprofen (for pain/fever)
- Intranasal decongestant or antihistamine (not for <6yo; caution in 6-12yo)
- Little evidence of effect but SEs (e.g. drowsiness)
- Limit decongestant use to 3-5d (rebound congestion)
Complications and prognosis of the common cold?
Complications:
- Otitis media
- Acute exacerbation of asthma
- Sinusitis
Self-limiting → symptoms clear in 7-10d
- Children may get back-to-back infections → may last longer
What is whooping cough (pertussis)?
A highly contagious respiratory tract infection caused by Bordatella pertussis
Aetiology of whooping cough (pertussis)?
Bordatella pertussis is a gram-negative bacillus which spreads through aerosolised droplets
- The bacteria attach to the respiratory epithelium and produce toxins à toxins paralyse the cilia and cause inflammation à leads to impaired clearance of respiratory secretions à cough
- Highly contagious à up to 90% household contacts develop the disease
RFs for whooping cough (pertussis)?
- non-vaccination
- exposure to an infected individual (esp during catarrhal phase)
- Also babies born to mothers who became infected at 34wks or later
Epidemiology of whooping cough (pertussis)?
It is an endemic, with epidemics every 3-4yrs
There is a vaccine but is still reasonably common
- Most common in >15yo but most severe in infants
Signs and symptoms of whooping cough (pertussis)?
-
Catarrhal phase:
- Lasts 1-2wks
- Coryzal symptoms → mimics other URTIs so rarely diagnosed at this stage
-
Paroxysmal phase:
- Lasts for 2-8wks; can last up to 3 months
- There are episodes of severe paroxysms of coughing followed by an inspiratory gasp (against a closed glottis), producing the classic ‘whoop’ sound
- Often worse at night; may cause vomiting; occasionally severe enough to cause cyanosis
- During a paroxysm, the child goes red/blue in the face; mucus flows from the nose/mouth
- Epistaxis & subconjunctival haemorrhages can occur after vigorous coughing
- In infants, the whoop may be absent but apnoea is common
- This is the time that complications frequently occur
-
Convalescent phase:
- Symptoms gradually decrease, but cough may persist for many months
-
Older children/adolescents may not have distinct stages
- Symptoms include uninterrupted coughing, feelings of suffocation, headaches
Ix for whooping cough (pertussis)?
-
If cough is <2wks from onset:
- Culture of a nasopharyngeal aspirate or nasopharyngeal swab
- PCR testing of a nasopharyngeal swab can also be done in severe illness → quicker results
- Sensitivity decreases if >2wks from cough onset
-
If cough is >2wks from onset:
- Anti-pertussis toxin IgG serology
- NB pertussis vaccine can produce a false positive
-
FBC
- Characteristically there is marked lymphocytosis (>15x109/L)
Mx for whooping cough (pertussis)?
Indications for hospital admission:
- <6 months of age and acutely unwell
- Significant breathing difficulties, e.g. apnoeic episodes, cyanosis, respiratory distress, severe paroxysms
- Feeding difficulties, vomiting with dehydration and weight loss
- Significant complications, e.g. pneumonia, seizures
Antibiotics:
- Eradicate the organism and reduce infectivity; only decrease symptoms if started during the catarrhal phase
- Macrolides
- Azithromycin or clarithromycin
- Co-trimoxazole (trimethoprim/sulfamethoxazole) is 2nd line (if macrolides not tolerated/resistance)
- Close contacts should receive macrolide prophylaxis
Further management is supportive:
- Paracetamol and ibuprofen
- Adequate fluid intake
- Isolate children (if admitted to hospital); avoid nursery/school until they have had cough for 21d or antibiotics for 5d
- Notifiable disease
Describe the vaccination schedule for whooping cough
- Given at 2, 3 and 4 months of age, with a booster at 3yrs and 4months
- Unimmunised infant contacts should be vaccinated
- Does not guarantee protection but reduces risk and severity; level of protection declines during childhood (but pertussis is much milder in adolescents and adults)
- Reimmunization during pregnancy in UK à reduces risk in the infant during the first few months of life
Complications and prognosis of whooping cough (pertussis)?
Complications:
- Otitis media (most common)
-
Pneumonia (20%)
- May be primary infection from Bordatella pertussis or secondary to other organisms
-
Seizures
- Due to cerebral hypoxia secondary to severe paroxysms of cough
- Apnoea (esp in infants)
- Bronchiectasis
- Rib fracture (more common in adolescents/adults)
Higher risk of complications and mortality in unvaccinated children <6mo (3.5% mortality)
What is croup?
A common viral respiratory disease of childhood, characterised by the sudden onset of a barking cough, often accompanied by stridor, voice hoarseness and respiratory distress
Aka laryngotracheobronchitis
How is croup classified?
Ix for croup?
- Clinical diagnosis
- Occasionally AP and lateral neck X-ray → steeple sign
Compare and contrast croup and epiglottitis
What is the pharmacological Mx of asthma?
What is the Mx of asthma exacerbation?
- ABCDE approach
- O2 if sats are <92%
-
SABA
- Given via inhaler and spacer, unless attack is severe to life-threatening when it is nebulised
- Burst therapy: 1 puff, 5-10 deep breaths, repeat up to 10 times à this is 1 burst
- Steroids (oral or IV)
- Ipratropium (nebulised/inhaled) – in severe
- IV salbutamol, aminophylline or magnesium sulphate – in severe
