Respiratory Flashcards
What is asthma?
What are the three key components to pathophysiology
Clinical diagnosis: reversible airflow limitation.
- Hyperresponsive airway (bronchial SM contraction to stimuli e.g. cold air, house dust mite, smoke)
- Bronchial inflammation (widespread inflammation in bronchioles, associated with oedema, smooth muscle hypertrophy, mucus plugging & epithelial damage - changes may be chronic, but more pronounced with exacerbation)
- Airflow limitation: usually reversible, either spontaneously or with treatment, but may be some chronic underlying changes
What cell changes are seen in asthma
Th2 infiltration / pathology (T lymphocytes)
Goblet cell infiltration
Infiltration of inflammatory cells e.g. CD4+ cells, eosinophils & mast cells.
Increased cytokines (IL-4, IL-5, IL-13).
What clinical findings may be seen in a patient with asthma (resp exam)?
- Wheeze (can be heard at bedside or require auscultation, however, volume can be misleading; quieter wheeze may be suggestive of severely narrowed airways. May also be absent in severe disease where insufficient airflow to generate wheeze - reduced air entry)
- Coughing (for some children may be main symptom – particularly at night, dry)
- SOB (if poorly controlled: may present with SOB showing increased respiratory effort on minimal exertion)
- Atopy: (most childhood asthma associated with element of atopic disease e.g. eczema, rhinitis, hay fever or family history of atopy - managing these diseases often improves asthma symptoms!)
- Chest wall remodelling: (rarely in severe disease children can develop pectus carinatum & Harrison’s sulcus may also be seen in chronic disease)
- Hyperexpanded chest
- Use of accessory muscles / increased work of breathing
What investigations should be done for suspected asthma?
- Spirometry (↓ FEV1 with preserved FVC: FEV1/FVC <70%). Pre and post 500mcg salbutamol.
- Peak flow: thought to correspond with FEV₁ & easier to perform (reasonable PEFR : FEV₁ correlation), but not used as much as spirometry. Also using bronchodilator.
- Exhaled nitric oxide test (FeNO test): higher fraction of NO in exhaled breath suggests poorly controlled eosinophilic inflammation (although literature suggests steroids does not correct this?)
- Allergy test: skin prick to aeroallergens or specific IgE to allergens suggests atopic nature & useful if considering aggravating environmental factors
If very severe & referred to tertiary centre, child may undergo further tests e.g. bronchoscopy, formal lung function tests and exhaled nitric oxide test (found to be increased with inflammatory conditions) before more novel therapies are considered
How is spirometry used to diagnose asthma?
Obstructive lung function: ↓ FEV1 with preserved FVC i.e. FEV1/FVC <70%
FEV₁ <80%,
FEV₁/FVC < 80%
≥12% increase in baseline FEV₁ post 500mcg salbutamol
Flow volume loop: concave phase of expiratory loop which improves with bronchodilator
How is peak flow used to diagnose asthma?
PEFR morning/evening variability >15% confirms diagnosis, especially if >15% response to 500mcg β agonist
Asthma unlikely if: completely normal values (for age), variability <5% & no bronchodilator response (peak flow generally useful for excluding)
What is the difference between transient early wheezers, and non-atopic wheezers?
Transient early wheezers: preschool children wheeze with colds but completely well between (~60% better by 6 yrs)
Non-atopic wheezers: children wheezy with colds & have interval symptoms (symptoms between exacerbations), night-time cough & wheeze on exertion – suggestive of airway hyperactivity)
What is the difference between episodic viral wheeze and multi-trigger wheeze?
EVW: exclusively triggered by viral respiratory tract infections (inhaled therapies have intermittent benefit during exacerbations but not required between illnesses, oral steroids have no benefit) - more common in preschool
MTW: also triggered by other precipitants e.g. allergens, exercise, tobacco smoke & suggested that MTW may be an indication of later allergic asthma and more likely to respond to asthma treatment than EVW
What are the 5 steps of chronic asthma management?
- SABA (salbutamol) as required
- Daily inhaled corticosteroids (200-400 mcg/day)
- <5 years: leukotriene receptor antagonist e.g. Montelukast tablets. >5 years: LABA e.g. salmeterol.
If still inadequate, increase corticosteroid up to 800mcg. - Addition of leukotriene receptor antagonist, increase inhaled corticosteroid dose (up to 2000mcg/day) or slow release theophylline
- Oral corticosteroids as maintenance therapy and maintain high dose inhaled corticosteroid.
Note: all are preventers except salbutamol (reliever).
What are some side effects of steroid treatment for asthma?
- INHALED corticosteroids generally more mild effects e.g. oral thrush. Can reduce growth velocity (regular mid-high dose may affect velocity by ~0.8cm/year): LTRAs do not have these side effects.
- If high-dose corticosteroids for prolonged periods, adrenal glands can stop producing glucocorticoids. Replace with hydrocortisone & plan to ↑ dose during periods of ill health & careful monitoring if vomiting or unable to tolerate oral intake (avoids Addisonian crisis).
Note: LTRAs may cause disturbed sleep
What are some non-pharmacological ways to manage asthma?
Aim to reduce treatment once control achieved: for atopic patient, home interventions e.g. damp wimping surfaces (↓ floating dust particles & house dust mite), protective bedding. Encourage parents to stop smoking (even if smoking outside, carried on clothing).
What clinical features are needed for asthma to be considered completely controlled?
no daytime symptoms no need for reliever medications with the exception of during exercise no asthma exacerbation no limitation on daily activity normal lung function minimal side effects from medication
What treatments are available for severe therapy-resistant asthmatics or more difficult asthma cases/
more novel therapies including:
- omalizumab (humanised antibody for atopic children)
- monthly corticosteroid injections
- beta-2-agonist subcutaneous infusions
- methotrexate
What is the criteria for a moderate asthma attack?
SpO2 ≥92%
PEFR >50% of best predicted
No clinical features of severe respiratory distress
What is the criteria for a severe asthma attack?
SpO₂ <92%
PEFR 33-50% of best predicted
Too breathless to talk & eat.
Accessory neck muscles
What is the criteria for a life-threatening asthma attack?
Sats <92% OR any of following..
PEFR of <33% of best predicted
Cyanosis Hypertension Exhuastion Silent chest Tachycardia
Poor respiratory effort, altered consciousness / confusion
How is a mild asthma exacerbation treated?
Inhaled therapy: 2-10 puffs salbutamol (titrated to response)
No corticosteroids
Monitor 4 hours, if stable send home with weaning regime (salbutamol dose given in ED gradually titrated over days)
If not stable after 4 hours, more frequent bronchodilator & monitoring in hospital.
How is a moderate-severe asthma exacerbation treated?
Inhaled therapy: 10 puffs salbutamol (or if oxygen required, through an oxygen-driven nebuliser )
Oral prednisolone
(If life-threatening, IV hydrocortisone)
Reassess after 20 minutes, if required: add ipratropium bromide to the nebulisers & keep monitoring response. Repeat nebulisers if required up to 3 further times ‘back to back’.
Oxygen requirement already necessitates admission. If no sustained improvement after 3 nebulisers, consider (if not already) IV salbutamol, magnesium sulphate or aminophylline
What are two types of inhaler?
Metered Dose Inhaler (MDI): pressurised inactive gas propels one dose of medication each time dose is released by pressing top of inhaler – should be used with spacer to maximise drug deposition (all children should use a spacer with an MDI!). Face mask should be attached to the spacer until the child is old enough or capable of holding the mouthpiece in their mouth & forming a seal around it.
Breath-activated inhaler: dose is triggered by breathing in at the mouthpiece
How are pre-school wheezing disorders managed?
Viral-induced episodic wheeze and multi-trigger wheeze: generally refers to under 5s who wheeze
Bronchodilators can be effective and frequency of exacerbations should be considered before starting inhaled corticosteroids for long-term control. Leukotriene receptor antagonists e.g. montelukast may be of benefit (start at onset of sneezing etc). No evidence for the use of corticosteroids in acute exacerbations.
What is bronchiolitis?
Who does it affect?
Inflammation of bronchioles
Obstructed with mucus compromising ventilation.
~1/3 children in first 2 years of life (~3% admitted).
Lower respiratory tract infection - almost always viral; most commonly respiratory syncytiovirus (RSV) but many other infections including adenovirus, human metapneumovirus and rhinovirus. These viruses are more prevalent in the winter months ‘bronchiolitis season’.
What is RSV? Who does it affect?
RSV = 65-85% cases of bronchiolitis
o Exposure universal by 3 years of age
o Incubation period 4 days
o Transmission by hand-nose and hand-eye contact
o Re-infection possible as early as few weeks post-recovery (can get bronchiolitis again!)
What features in the history suggests a child has bronchiolitis?
- Exposure to older child / adult with minor respiratory disease
- Mild URTI: serous nasal discharge / sneezing.
- 2-5 days later: cough, SOB, wheezy, irritability, decreased appetite & bottle feeding difficulties.
- Cough: dry cough, episodic, often resulting in vomiting (may be preceding signs of URTI)
- Respiratory distress: tachypnoea, head bobbing, tracheal tug, subcostal/intercostal recession, dramatic abdominal movements
- Pyrexia: low-grade fever common due to the viral illness
- Poor feeding: predominantly infants, major consideration to whether admission or further intervention needed (for non-ambulatory infant, feeding most energetic activity of daily routine, if already tired from breathing alone, often have no energy to feed).
Occasionally: periodic breathing, apnoea, ?SIDS (apnoea: serious complication - breathing pauses especially when sleeping)
What findings may be seen on examination of a child with bronchiolitis?
Minimal / no fever (<10% febrile on admission)
Nasal congestion +/- flaring
Irritable
Dehydration possible
Tachypnoea
IC & SC recession
Reduced air entry bilaterally (suggestive of consolidation or collapse)
Widespread fine crepitations / crackles throughout chest
Prolonged expiratory phase with wheeze
What investigations can be done for bronchiolitis?
Clinical diagnosis. However, investigations can include..
- Nasopharyngeal aspirates (NPA) for viral PCR / immunofluorescence (rapid same day test: identifies virus, rarely influences immediate management but can be useful for cohorting reduce cross-infection. adenoviruses can cause more long-term sequalae – may be more cautious. can also help if e.g. higher fever than expected – if grow RSV can confirm do have bronchiolitis).
- Blood gas: assesses ventilation, particularly if requiring respiratory support
- CXR: rarely required unless asymmetric chest sounds heard & therefore different or concurrent pathology suspected – may be associated with lobar collapse, pneumothorax or superimposed pneumonia
- Bloods: may have ↑WCC &CRP but unlikely to influence mgmt: high CRP in neonate may trigger LP to exclude meningitis. ↑lymphocytes may suggest whooping cough if other features present, U&Es can help identify hydration status.
Differential diagnoses for bronchiolitis?
Bacterial infection (note: this is also a recognised comorbidity as bronchiolitis can leave child susceptible to opportunistic bacteria), GORD with aspiration, heart failure, pneumothorax, collapsed lung
How can bronchiolitis be prevented?
No direct prevention / vaccine but winter monthly Palivizumab injection (specific Ig against RSV) recommended for high risk young children e.g. congenital cardiac disease, chronic lung disease (on non-invasive ventilation; for cost-benefit as if on ventilation would end up in PICU), immunodeficiencies & ex-premature.
When would you admit a child with bronchiolitis?
- Not drinking / feeding (< 2/3rds normal intake & dehydration)
- High fever (39+) – think other complications & secondary infections
- Requirement for oxygen (i.e. SaO₂ <92%),
- Other risk factors (particularly very young): congenital heart disease, immunodeficiencies, chronic lung disease, ex-premature requiring home oxygen
NICE recommendations
Immediate referral (usually 999) if apnoea, looks seriously unwell to professional, severe distress e.g. grunting, marked chest recession, RR >70, central cyanosis, persistent SaO2 <92%
Consider referral if RR >60, difficulty breastfeeding or inadequate oral fluid intake (50-75% of usual volume ‘taking account of risk factors’ & using clinical judgement’), clinical dehydration
How is bronchiolitis managed?
- Minimal handling (distress to baby may exacerbate respiratory distress – blood gases and other blood tests should be performed sparingly)
- Oxygen & ventilation: ability to maintain >92% on RA usually main indicator for admission
some babies require more invasive support (still desaturating on oxygen)- step-wise progression: nasal cannula oxygen –> high flow e.g. optiflow / vapotherm (may offset effort of breathing) –> CPAP –> intubation & conventional ventilation
- Hydration support: feeding may be compromised if significant demand of ventilation: bottles (little & often) –> NG tube –> if not tolerated - IV fluids.
- Apnoea monitoring (particularly if <3/12)
- Inhaled therapies (controversial): nebulised NaCl isotonic (0.9%) or hypertonic (3%): Cochrane: no benefit of hypertonic), salbutamol (unlikely to benefit as most children <6 months have no β2 receptors & wheeze more likely due to mucus; but sometimes they are still tried) or ipratropium bromide.
Inhaled therapy may be more effective if:
• FHx atopic conditions
• Co-existent eczema
• > 6 months
What are complications of bronchiolitis?
Lung collapse, superadded pneumonia, respiratory failure. Rarely: those with severe infection develop chronic non-reversible obstructive lung disease (bronchiolitis obliterans) due to scarring & fibrosis of small airways.
What is the general prognosis of bronchiolitis?
Peak at 3-5 days before starting to improve; vast majority won’t need intervention and cared for at home.
Often, dry persistent cough for several weeks.
Some will require admission for supportive measures during acute phase and very small number go on to need ventilator support.
What is suggestive of mild, moderate or severe respiratory distress?
Mild: tachypnoea + SOB
Mod: subcostal retractions + nasal flaring
Severe: supraclavicular tugging + head bobbing
What are the signs of respiratory distress?
Tachypnoea
Intercostal & sternal recession (particularly significant if >6-7 years)
Accessory muscles (head bobbing in infants)
Tracheal tug
Tripoding / anchoring
Nasal flaring (particularly seen in infants)
Stridor (upper airway obstruction)
Wheezing (usually smaller-calibre lower airway obstruction)
Grunting (exhalation against partially closed glottis to ↑ end expiratory pressure– severe respiratory distress in infants)
What is cystic fibrosis? (epidemiology, pathophysiology)
Autosomal recessive: 1 in 25 carrier rate. UK incidence 1:2000 (most common genetic disease in Europe). 1000s known mutations: p.Phe508del (ΔF508) most common in UK Caucasian population (~85% cases): chromosome 7
Defective cystic fibrosis transmembrane conductance regulator (CFTR): responsible for efflux of Cl + inhibition of adjacent epithelial sodium channel (eNaC). If no Cl pumped out, sodium floods in uninhibited > high osmolality > water into cell > thick, dehydrated mucus (hyperviscous) builds up in lumens throughout body.
What clinical features may be seen in a patient with CF?
- Chest infections (pseudomonas common - thick mucus build up prevents bacteria clearance). Recurrent infections > scarring or BRONCHIECTASIS (due to damage to lung tissue) + ultimately resp. failure if untreated.
- Faltering growth / failure to thrive
- Pancreatic insufficiency > failure to digest fat > steatorrhoea
- Salt depletion > dehydration
- Higher energy expenditure (metabolic rate) for fighting infection & supporting elevated respiratory effort - Nasal obstruction / polyps (10-40% of cases, uncommon if <5 years). Enlarged polyps can obstruct nasal passage affecting sense of smell + taste, CF should be ruled out in any child with polyps
- Bowel obstruction: may present in neonatal period (20%): meconium ileus, or later in childhood: distal intestinal obstruction syndrome (DIOS)
- Pressure from trying to push matter out can also result in rectal prolapse - Digital clubbing
What investigations are done for CF?
Immune-reactive trypsinogen (IRT) levels: UK newborn screening program (day 5). If IRT elevated, referred to centre for sweat test + counselling.
Sweat test (gold standard): chloride content >60nmol/L confirms diagnosis, if 40-60nmol/L further investigation required
Genetic tests: look for mutations & may direct therapy
Pancreatic function (faecal elastase): next priority - absence of elastase in faecal matter suggests pancreatic insufficiency
