Respiratory

Question 1

What is bronchopulmonary dysplasia?

Answer 1

a form of chronic lung disease that affects newborns, most often those who are born prematurely and need oxygen therapy. In BPD the lungs and the airways (bronchi) are damaged, causing tissue destruction (dysplasia) in the tiny air sacs of the lung (alveoli)

Abnormal pul development,
Prolonged mechanical ventilation
↓alveoli no, interstitial thickening, abnormal pul vasculature development, pul oedema + atelectasis.

Question 2

Features of bronchopulmonary dysplasia?

Answer 2

Severe retractions

Audible rales, crackles

Intermittent expiratory wheeze if airway narrow from scar formation, constriction, mucus retention, collapse/ oedema.

O2 desats during feeds

Asthma in childhood

Question 3

Complications of bronchopulmonary dysplasia?

Answer 3

Resp distress 
Ventilator dependence, pul hypotension, subglottic stenosis 
Feeding problems poor weight gain 
Severe bronchiolitis, GORD
Low IQ > CP

Question 4

Investigations for bronchopulmonary dysplasia?

Answer 4

O2 ↓ test, need for O2 supplementation. O2 sats <90% within 60 mins of being placed in room air.

CXR: diffuse haziness, exudative fluid, multicystic sponge like, areas pf alternating oedema, pul scarring emphysema, Hyperinflation, rounded radiolucent mass alternating with thin denser lines

Histology: necrotising bronchiolitis with alveolar fibrosis

Question 5

Management of bronchopulmonary dysplasia?

Answer 5

Supportive

Nutritional supplementation

Fluid restriction

Diuretics

O2

Gentle ventilation low vol/ O2 conc

Steroids

Surfactant

Almost all weaned by 1 yr ↑ risk of bronchiolitis > give palivizumab monthly + LT risk of COPD

Question 6

What is neonate respiratory distress syndrome?

Answer 6

happens when a baby’s lungs are not fully developed and cannot provide enough oxygen, causing breathing difficulties. It usually affects premature babies.

not enough surfactant, so lungs collapsing, progressive + diffuse atelectasis

Damage of epithelial cells can be permanent
24-28 wks deffo. 50% at 32 wks

RF - premature, mother DM, LBW, lungs not properly developed, 2nd twin, CS, 2’ to other pulmonary pathology > meconium, perinatal asphyxia, pul hypoxia

Question 7

Features of neonate respiratory distress syndrome?

Answer 7

Worsening tachypnoea >60/min 1st 4 hrs of birth

↑inspiratory effort

Grunting

Flaring of nostrils

Intercostal recession

Cyanosis

Resp failure, reinfilation between breaths makes baby very tired.

Question 8

Complications of neonate respiratory distress syndrome?

Answer 8

Death

Pneumothorax: prolonged pressure from ventilation

Hypoglycaemia, acidosis + systemic compromise.

Chronically: BPD, IVH, retinopathy of prematurity

Question 9

Investigation and management of neonate respiratory distress syndrome?

Answer 9

CXR: diffuse granular patterns, air bronchograms, low lung volume, ground glass, heart border indistinct Pneumothoraxes.

ABG: hypoxaemia, hypercapnia

Prevention: beta/dexamethasone prenatally. If postnatal risk of GI bleed, intestinal perf, hypoglycaemia, HBP, HCM, poor growth.

CPAP, intubation, intratraceal surfactant therapy

Question 10

What is pulmonary hypoplasia?

Answer 10

a condition in which the lungs are abnormally small, and do not have enough tissue and blood flow to allow the baby to breathe on his or her own.

Causes - Oligohydramnios, PROM, congenital diaphragmatic hernia

Underdeveloped lungs, ↓no/ size of bronchopul seg/ alveoli

Potter’s: bilat renal agenesis, oligohydramnios, low set ears, beaked nose, ↓lung expansion, ↓mechanical stretching

SOL: diaphragmatic hernia, congen cyst adenomatoid formation, fetal hydronephrosis, mediastinal tumour, caudal regression syndrome, dextrocardia, sacrococcygeal teratoma.

Question 11

Features of pulmonary hypoplasia?

Answer 11

Infants with persistent tachypnoea ± feeding difficulties
Poor fetal movement, AF leakage, oligohydramnios
Asymptomatic
Severe resp distress
Small bell shaped chest
Heart displacement
↓/absent BS

Question 12

Investigations and management of pulmonary hypoplasia?

Answer 12

Fetal USS

Amnioinfusion: instilling isotonic fluid into amniotic cavity

Amniopatch: intra-amniotic injection of plt cryoprecipitate, seal amniotic fluid leak

Resp support

Question 13

What is croup?

Answer 13

a form of upper respiratory tract infection seen in infants and toddlers.

It is characterised by stridor which is caused by a combination of laryngeal oedema and secretions.

Parainfluenza viruses account for the majority of cases. Other causes - RSV, adenovirus, Diptheria

6m-3yrs

more common in autumn

Question 14

Features of croup?

Answer 14

stridor
barking cough (worse at night)
fever
coryzal symptoms

Question 15

Severity of croup?

Answer 15

Mild
Occasional barking cough
No audible stridor at rest
No or mild suprasternal and/or intercostal recession
The child is happy and is prepared to eat, drink, and play

Moderate
Frequent barking cough
Easily audible stridor at rest
Suprasternal and sternal wall retraction at rest
No or little distress or agitation
The child can be placated and is interested in its surroundings

Severe
Frequent barking cough
Prominent inspiratory (and occasionally, expiratory) stridor at rest
Marked sternal wall retractions
Significant distress and agitation, or lethargy or restlessness (a sign of hypoxaemia)
Tachycardia occurs with more severe obstructive symptoms and hypoxaemi

Question 16

When to admit a child with croup?

Answer 16

Moderate or severe croup

< 6 months of age

known upper airway abnormalities (e.g. Laryngomalacia, Down’s syndrome)

uncertainty about diagnosis (important differentials include acute epiglottitis, bacterial tracheitis, peritonsillar abscess and foreign body inhalation)

Question 17

Investigations for croup?

Answer 17

the vast majority of children are diagnosed clinically

however, if a chest x-ray is done:
a posterior-anterior view will show subglottic narrowing, commonly called the ‘steeple sign’

in contrast, a lateral view in acute epiglottis will show swelling of the epiglottis - the ‘thumb sign’

Westley scale 0-17 - mainly for research, not clinically
3-7: moderate
8-11: severe
12+: resp failure

Question 18

Management of croup?

Answer 18

CKS recommend giving a single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity

prednisolone is an alternative if dexamethasone is not available

humidified O2

fluids, antipyretics

Emergency treatment
high-flow oxygen
nebulised adrenaline
intubation if impending respiratory failure

Question 19

What is acute epiglottitis?

Answer 19

Fluid, inflam cell accumulation, rapid progressive swelling of epiglottis, supraglottic larynx, airway narrows, ball-valve curling.

Haem influenzae type B

RF: unimmunised, mucosal trauma (burns, caustic substance, FBI), 6-12y/o, DM, substance abuse, BMI >25

Don’t agitate child incl attempt to examine throat = can precipitate obstruction

Question 20

Features of acute epiglottitis?

Answer 20

rapid onset

high temperature, generally unwell

stridor

drooling of saliva

‘tripod’ position: the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position

3D’s - dysphagia, drooling, distress

Question 21

Diagnosis of acute epiglottitis?

Answer 21

made by direct visualisation (only by senior/airway trained staff)

However, x-rays may be done, particularly if there is concern about a foreign body:
a lateral view in acute epiglottis will show swelling of the epiglottis - the ‘thumb sign’
in contrast, a posterior-anterior view in croup will show subglottic narrowing, commonly called the ‘steeple sign’

Question 22

Management of acute epiglottitis?

Answer 22

immediate senior involvement, including those able to provide emergency airway support (e.g. anaesthetics, ENT)
> endotracheal intubation > may be necessary to protect the airway

if suspected do NOT examine the throat due to the risk of acute airway obstruction

the diagnosis is made by direct visualisation but this should only be done by senior staff who are able to intubate if necessary

oxygen - humidified in severe intubation, if not possible then cricothyroidotomy

intravenous antibiotics - Cefotaxime, ceftriaxone, clinda/ vancomycin. Pen allergic: chloramphenicol

Oral Abx - co-amoxiclav, cefaclor

IV steroids - reduce swelling

Hib vaccine

Question 23

What is laryngomalacia?

Answer 23

Congenital abnormality of the larynx. aryepiglottic folds shorter than normal, cause folding of epiglottis in omega shape that prolapses during inspiration.

Infants typical present at 4 weeks of age with:
stridor

Question 24

Features of laryngomalacia?

Answer 24

Inspiratory stridor more marked when upset/ feeding

Noisy resps

Breathing difficulties

Impaired growth + development caused by hypoventilation

GO reflux

Swallowing problem + choking

Question 25

Investigation and management of laryngomalacia?

Answer 25

Laryngoscopy or bronchoscopy - omega shaped epiglottis Can resolve spont as throat muscles strengthen by age 2 Supplemental O2 if hypoxemic Surgical Tx: tracheotomy or supraglottoplasty

Question 26

What is whooping cough?

Answer 26

an infectious disease caused by the Gram-negative bacterium Bordetella pertussis. It typically presents in children. There are around 1,000 cases are reported each year in the UK. infants are routinely immunised at 2, 3, 4 months and 3-5 years. Newborn infants are particularly vulnerable, which is why the vaccination campaign for pregnant women was introduced - Women who are between 16-32 weeks pregnant will be offered the vaccine. neither infection nor immunisation results in lifelong protection - hence adolescents and adults may develop whooping cough despite having had their routine immunisations

Question 27

Features of whooping cough?

Answer 27

2-3 days of coryza precede: coughing bouts: usually worse at night and after feeding, may be ended by vomiting & associated central cyanosis inspiratory whoop: not always present (caused by forced inspiration against a closed glottis) infants may have spells of apnoea persistent coughing may cause subconjunctival haemorrhages or even anoxia leading to syncope & seizures symptoms may last 10-14 weeks* and tend to be more severe in infants marked lymphocytosis

Question 28

Diagnostic criteria of whooping cough?

Answer 28

Whooping cough should be suspected if a person has an acute cough that has lasted for 14 days or more without another apparent cause, and has one or more of the following features: Paroxysmal cough. Inspiratory whoop. Post-tussive vomiting. Undiagnosed apnoeic attacks in young infants

Question 29

Investigations for whooping cough?

Answer 29

per nasal swab culture for Bordetella pertussis - may take several days or weeks to come back PCR and serology are now increasingly used as their availability becomes more widespread

Question 30

Complications of whooping cough?

Answer 30

subconjunctival haemorrhage pneumonia bronchiectasis seizures

Question 31

Management of whooping cough?

Answer 31

infants under 6 months with suspect pertussis should be admitted in the UK pertussis is a notifiable disease an oral macrolide (e.g. clarithromycin, azithromycin or erythromycin) is indicated if the onset of the cough is within the previous 21 days to eradicate the organism and reduce the spread household contacts should be offered antibiotic prophylaxis antibiotic therapy has not been shown to alter the course of the illness school exclusion: 48 hours after commencing antibiotics (or 21 days from onset of symptoms if no antibiotics )

Question 32

What is bronchiolitis?

Answer 32

a condition characterised by acute bronchiolar inflammation. > epithelial cells produce mucus, BVs vasodilate, leaky. Inflam + swelling, walls thicker + airway narrows. Dead cells + mucus in airway, mucus plugs, air trapping. Air diffuse into blood, atelectasis. Over inflation of lungs. Respiratory syncytial virus (RSV) is the pathogen in 75-80% of cases. other causes - mycoplasma, adenoviruses. may be secondary bacterial infection most common cause of a serious lower respiratory tract infection in < 1yr olds (90% are 1-9 months, with a peak incidence of 3-6 months). Maternal IgG provides protection to newborns against RSV higher incidence in winter more serious if bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis RF - <2, prev infection, daycare, ↓immunity, NM disorders, premie, CV malformation, airway malformation, smoking

Question 33

Features of bronchiolitis?

Answer 33

coryzal symptoms (including mild fever) precede: dry cough increasing breathlessness wheezing, fine inspiratory crackles (not always present) feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission

Question 34

When to immediately refer for bronchiolitis?

Answer 34

apnoea (observed or reported) child looks seriously unwell to a healthcare professional severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute central cyanosis persistent oxygen saturation of less than 92% when breathing air.

Question 35

When to consider referring to hospital with bronchiolitis?

Answer 35

a respiratory rate of over 60 breaths/minute difficulty with breastfeeding or inadequate oral fluid intake (50-75% of usual volume 'taking account of risk factors and using clinical judgement') clinical dehydration.

Question 36

Investigation for bronchiolitis?

Answer 36

X-ray: atelectasis, patchy infiltrates, hyperinflation Pos rapid viral testing Largely clinical immunofluorescence of nasopharyngeal secretions may show RSV

Question 37

Management of bronchiolitis?

Answer 37

humidified oxygen is given via a head box and is typically recommended if the oxygen saturations are persistently < 92% nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth suction is sometimes used for excessive upper airway secretions Palivizumab: monoclonal Ig against RSV given monthly from RSV season for prematurely born infants, CLD, CHD Paracetamol, ibuprofen Intubation Almost all recover, rarely progresses to broncholitis obliterans, permanent scarring of bronchioles, chronic cough/ wheeze

Question 38

What is asthma?

Answer 38

↑airway responsiveness, reversible airway obstruction Bronchoconstriction, smooth muscles of bronchioles spasm/ contract, mucus hypersecretion impaired mucociliary function, difficulty breathing. Vasodilation of pul vasculature, cap permeability, oedema. Triggers: air pollution, smoke, dust pet dander, cockroaches, mould, pollen, meds (aspirin, BB), faeces of dust mites, food eg peanut, wheat, industrial chemicals, infections. RF: allergic sensitisation, atopic resp viral infections in early life (RSV or human rhinovirus), serum eosinophilia, FH, active / passive smoking, F>M, obesity, acid suppressing drugs in pregnancy, GORD, OSA. Chronic: irreversible damage, smooth muscle hypertrophy, scarring + fibrosis, thickening of epithelial BM, narrows airway.

Question 39

Features of asthma?

Answer 39

Cough/ dyspnoea: precipitated by allergen exposure, cold air, smoke Worse with laughing. May wake pts. Dry night cough Recent URTI Chest tightness, dyspnoea, difficulty breathing, wheezing Curschmann spiral in sputum: spiral shaped mucus plugs, casts from small bronchi, blocks air exchange + inhaled meds from reaching inflam Charcot-Leyden crystals sputum: needle shaped, breakdown of eosinophils Tachypnoea, hyperinflated chest Hyperresonant Nasal polyps Dyspnoea on exertion Harrison’s sulci: rib deformity at insertion of diaphragm muscle caused by chronic resp difficulty

Question 40

Complications of asthma?

Answer 40

Severe exacerbations Airway remodelling Oral candidiasis: 2° to use of ICS Dysphonia: 2° to use of ICS, laryngeal muscle spasms Pneumothorax/ pneumomediastimum Resp failure Stunted growth due to steroids

Question 41

Investigations for asthma?

Answer 41

FEV1:FVC <80% predicted Reversibility: prebronchodilator spirometry (withhold SABA 4hrs, LABA 15 hrs), 15 mins after salbutamol. FEV-1 ^ by 200mls + 12% FBC: ^IgE, neutrophilia, eosinophila. Skin prick testing for allergies. Sputum eosinophilia <3% Niox machine: >40 Peak flow: exagg variation. Mannitol challenge test: acts on inflam cells trigger release of mediators, cause bronchoconstriction in those with hyperreactivity. Do spirometry, inhale 🡩 conc of mannitol. Spirometry each time. When FEV1 🡫 15% of baseline define what degree of bronchial hyperreactivity Attempt to measure PEF in all children aged > 5 years

Question 42

Management of asthma in children?

Answer 42

Step 1: SABA Step 2: if using >1 a day. ICS low dose Step 3: add LTRA Theophylline/ zileuton, montelukast, zafirulast, sodium cromoglicate, nedocromil. Step 4: add LABA, Review if should continue LTRA. Step 5: SABA + switch ICS/LABA for maintenance + reliever therapy that includes paediatric low dose ICS. Step 6: mod dose MART Step 7: SABA + 1 of following, ↑ICS to paed high dose, either fixed dose regime or MART, trial additional drug e.g. theophylline, refer. If child <5: 1st SABA 2nd: SABA + 8 wk trial of mod dose ICS, if don’t resolve review whether alternative diagnosis likely, if Sx resolved then reoccurred within 4wks of stopping ICS, restart ICS at paed low dose as maintenance. If Sx reoccurred beyond 4 wks stopping ICS, repeat 8 wk trial of paediatric mod dose of ICS. 3rd SABA, paediatric low dose ICS + LTRA. 4th stop LTRA + refer to paediatric asthma specialist

Question 43

Features of moderate asthma attack?

Answer 43

SpO2 > 92% PEF > 50% best or predicted No clinical features of severe asthma

Question 44

Features of severe asthma attack?

Answer 44

``` SpO2 < 92% PEF 33-50% best or predicted Can't complete sentences in one breath or too breathless to talk or feed HR> 125/min RR > 30/min Use of accessory neck muscles ```

Question 45

Features of life-threatening asthma?

Answer 45

``` SpO2 <92% PEF <33% of best or predicted Silent chest Poor respiratory effort Altered consciousness Cyanosis ```