Respiratory Flashcards

1
Q

What is bronchopulmonary dysplasia?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Features of bronchopulmonary dysplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Complications of bronchopulmonary dysplasia?

A
Resp distress 
Ventilator dependence, pul hypotension, subglottic stenosis 
Feeding problems poor weight gain 
Severe bronchiolitis, GORD
Low IQ > CP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigations for bronchopulmonary dysplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Management of bronchopulmonary dysplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is neonate respiratory distress syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Features of neonate respiratory distress syndrome?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Complications of neonate respiratory distress syndrome?

A

Death

Pneumothorax: prolonged pressure from ventilation

Hypoglycaemia, acidosis + systemic compromise.

Chronically: BPD, IVH, retinopathy of prematurity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Investigation and management of neonate respiratory distress syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is pulmonary hypoplasia?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Features of pulmonary hypoplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Investigations and management of pulmonary hypoplasia?

A

Fetal USS

Amnioinfusion: instilling isotonic fluid into amniotic cavity

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

Resp support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is croup?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Features of croup?

A

stridor
barking cough (worse at night)
fever
coryzal symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Severity of croup?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When to admit a child with croup?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Investigations for croup?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Management of croup?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is acute epiglottitis?

A

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

20
Q

Features of acute epiglottitis?

A

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

21
Q

Diagnosis of acute epiglottitis?

A

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’

22
Q

Management of acute epiglottitis?

A

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

23
Q

What is laryngomalacia?

A

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

24
Q

Features of laryngomalacia?

A

Inspiratory stridor more marked when upset/ feeding

Noisy resps

Breathing difficulties

Impaired growth + development caused by hypoventilation

GO reflux

Swallowing problem + choking

25
Q

Investigation and management of laryngomalacia?

A

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

26
Q

What is whooping cough?

A

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

27
Q

Features of whooping cough?

A

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

28
Q

Diagnostic criteria of whooping cough?

A

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

29
Q

Investigations for whooping cough?

A

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

30
Q

Complications of whooping cough?

A

subconjunctival haemorrhage
pneumonia
bronchiectasis
seizures

31
Q

Management of whooping cough?

A

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 )

32
Q

What is bronchiolitis?

A

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

33
Q

Features of bronchiolitis?

A

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

34
Q

When to immediately refer for bronchiolitis?

A

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.

35
Q

When to consider referring to hospital with bronchiolitis?

A

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.

36
Q

Investigation for bronchiolitis?

A

X-ray: atelectasis, patchy infiltrates, hyperinflation

Pos rapid viral testing

Largely clinical

immunofluorescence of nasopharyngeal secretions may show RSV

37
Q

Management of bronchiolitis?

A

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

38
Q

What is asthma?

A

↑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.

39
Q

Features of asthma?

A

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

40
Q

Complications of asthma?

A

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

41
Q

Investigations for asthma?

A

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

42
Q

Management of asthma in children?

A

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

43
Q

Features of moderate asthma attack?

A

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

44
Q

Features of severe asthma attack?

A
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
45
Q

Features of life-threatening asthma?

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