Respiratory Flashcards
1
Q
What is asthma?
What are the three key components to pathophysiology
A
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
2
Q
What cell changes are seen in asthma
A
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).
3
Q
What clinical findings may be seen in a patient with asthma (resp exam)?
A
- 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
4
Q
What investigations should be done for suspected asthma?
A
- 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
5
Q
How is spirometry used to diagnose asthma?
A
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
6
Q
How is peak flow used to diagnose asthma?
A
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)
7
Q
What is the difference between transient early wheezers, and non-atopic wheezers?
A
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)
8
Q
What is the difference between episodic viral wheeze and multi-trigger wheeze?
A
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
9
Q
What are the 5 steps of chronic asthma management?
A
- 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).
10
Q
What are some side effects of steroid treatment for asthma?
A
- 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
11
Q
What are some non-pharmacological ways to manage asthma?
A
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).
12
Q
What clinical features are needed for asthma to be considered completely controlled?
A
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
13
Q
What treatments are available for severe therapy-resistant asthmatics or more difficult asthma cases/
A
more novel therapies including:
- omalizumab (humanised antibody for atopic children)
- monthly corticosteroid injections
- beta-2-agonist subcutaneous infusions
- methotrexate
14
Q
What is the criteria for a moderate asthma attack?
A
SpO2 ≥92%
PEFR >50% of best predicted
No clinical features of severe respiratory distress
15
Q
What is the criteria for a severe asthma attack?
A
SpO₂ <92%
PEFR 33-50% of best predicted
Too breathless to talk & eat.
Accessory neck muscles
16
Q
What is the criteria for a life-threatening asthma attack?
A
Sats <92% OR any of following..
PEFR of <33% of best predicted
Cyanosis Hypertension Exhuastion Silent chest Tachycardia
Poor respiratory effort, altered consciousness / confusion
17
Q
How is a mild asthma exacerbation treated?
A
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.
18
Q
How is a moderate-severe asthma exacerbation treated?
A
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
19
Q
What are two types of inhaler?
A
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
20
Q
How are pre-school wheezing disorders managed?
A
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.
21
Q
What is bronchiolitis?
Who does it affect?
A
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’.
22
Q
What is RSV? Who does it affect?
A
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!)
23
Q
What features in the history suggests a child has bronchiolitis?
A
- 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)
24
Q
What findings may be seen on examination of a child with bronchiolitis?
A
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
25
What investigations can be done for bronchiolitis?
Clinical diagnosis. However, investigations can include..
1. 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).
2. Blood gas: assesses ventilation, particularly if requiring respiratory support
3. CXR: rarely required unless asymmetric chest sounds heard & therefore different or concurrent pathology suspected – may be associated with lobar collapse, pneumothorax or superimposed pneumonia
4. 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.
26
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
27
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.
28
When would you admit a child with bronchiolitis?
1. Not drinking / feeding (< 2/3rds normal intake & dehydration)
2. High fever (39+) – think other complications & secondary infections
3. Requirement for oxygen (i.e. SaO₂ <92%),
4. 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
29
How is bronchiolitis managed?
1. Minimal handling (distress to baby may exacerbate respiratory distress – blood gases and other blood tests should be performed sparingly)
2. 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
3. Hydration support: feeding may be compromised if significant demand of ventilation: bottles (little & often) --> NG tube --> if not tolerated - IV fluids.
4. Apnoea monitoring (particularly if <3/12)
5. 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
30
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.
31
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.
32
What is suggestive of mild, moderate or severe respiratory distress?
Mild: tachypnoea + SOB
Mod: subcostal retractions + nasal flaring
Severe: supraclavicular tugging + head bobbing
33
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)
34
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.
35
What clinical features may be seen in a patient with CF?
1. 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.
2. 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
3. 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
4. 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
5. Digital clubbing
36
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
37
What are differential diagnoses for CF?
Once CF ruled out, recurrent chest infections should include assessment of immune system & consider other suppurative lung diseases e.g. PCD. Poor weight gain / nutritional elements could be coeliac disease, thyroid disease or any chronic childhood illness.
38
What long-term monitoring can be done for patients with CF?
Sputum analysis
Serial CXRs: low sensitivity for early changes in CF, however, may show hyperinflation, lobar collapse or bronchiectasis
High resolution CT (HRCT): much greater sensitivity for picking up CF changes – e.g. bronchial wall and/or peri-bronchial interstitial thickening & mucus plugging as well as features of bronchiectasis
Abdominal USS: signs of liver disease
Bone density scans
Methods for monitoring insulin function e.g. GTT
Bronchoscopy: can be used to obtain sputum samples to look for infection
39
Broadly speaking, how is CF managed (long-term)?
Multidisciplinary (physio + dietician)
1. Regular physiotherapy (several times a day)
2. Careful monitoring of nutritional status
Medications
1. Prophylactic Abx (some require regular admission for scheduled IV Abx to maintain health)
2. Mucolytics (clearance)
3. Airway: bronchodilators e.g. salbutamol (particularly effective if concurrent asthma) and inhaled corticosteroids may have prophylactic role if concurrent asthma
4. Nutritional support including pancreatic enzyme supplementation e.g. Creon (oral enzyme replacement for pancreatic exocrine function): required in ~80% of cases
5. Individual & family psychological input
6. Small molecule therapy
40
How are acute infective exacerbations of CF managed?
Aggressive treatment & may need supplementary oxygen.
Positive sputum cultures allow tailoring of Abx (usually continued until symptoms resolved e.g. increased sputum production).
If pseudomonas: dual therapy with broad spectrum B-lactam or cephalosporin + aminoglycoside (2 weeks oral ciprofloxacin, if not effective: admit for IV dual therapy e.g. tobramycin & ceftazidime: tobramycin requires trough levels as narrow therapeutic index)
Pseudomonas associated with ↑ decline in lung function, admission rate & mortality. Biofilm: once pseudomonas found, difficult to eradicate (near impossible once fully established): therefore oral ciprofloxacin (~3 weeks) & nebulised colomycin (~3 months) – repeat if grown again & may change nebulised antibiotics or give IV Abx (2 weeks)
41
What prophylactic Abx are given in CF?
Flucloxacillin (staphylococcus aureus prevention)
Nebulised antibiotics e.g. colomycin (pseudomonas aeruginosa prevention). If chronically colonised with pseudomonas (i.e. cultured >2x in year): regular prophylactic nebulisers (e.g. colomycin)
For most bacterial infections: 2 weeks oral Abx, if not improving > 2 weeks IV
Oral antifungals (e.g. aspergillus prevention)
42
What medications are used to help clearance in CF (mucolytics)?
Nebulised hypertonic NaCl draws fluid into airways, thins secretions
Nebulised DNase (e.g. dornase alfa) – breakdown of respiratory secretions, start everyone around age 6 & sometimes younger children
Oral mannitol but less evidence for this
43
What nutritional support is given to patients with CF?
1. Pancreatic enzyme supplements e.g. Creon (oral replacement) required ~80% cases
2. High calorie (not low fat) diet! - gastrostomy inserted if necessary for nutrition as appetite may not match increased calorific requirement
3. Micronutrient supplements e.g. Vitamin A, D, E & K (fat soluble vitamins particularly important due to fat malabsorption; i.e. not vitamin C)
4. Histamine receptor antagonist e.g. ranitidine & proton pump inhibitors e.g. omprazole (lower stomach pH reduces risk of Creon becoming denatured i.e. ↑ its absorption)
5. Insulin (treatment of CF-related diabetes)
44
What small molecule therapies are available for patients with CF?
New therapies for treating defective protein:
1st - (Ivacaftor) licenced for gating mutations (e.g. p.Gly551Asp i.e. G551D; found in ~5%) where CFTR molecule created & inserted into cell but does not open sufficiently. Restores degree of normal function & improves weight gain, 10% increase in lung function, ↓ exacerbation rates & returns sweat chlorides to normal. (£150,000/patient/year but approved by NICE; ~300 patients in UK).
New medicine may help with more common 508 mutation (for 4000 patients in country). Used in combination with Orkambi (a combination of ivacaftor - opens channel & lumacaftor – gets protein to surface better); not yet approved by NICE.
45
What are the complications of CF?
UK life expectancy: ~37 (median 41) but increasing (studies suggest ~50 years). Death usually due to respiratory failure, however, childhood death is uncommon
CF-related diabetes (in addition to exocrine function, endocrine function can also deteriorate > relative insulin deficiency > high fasting glucose – can be controlled in early stages with relatively small amounts of long-acting insulin). Prolonged uncontrolled hyperglycaemia can result in deteriorating lung function & poor weight gain.
CF-related liver disease: blockages throughout liver drainage architecture > hepatomegaly + portal hypertension. Some children require serial endoscopy & treatment of oesophageal varices.
Infertility: majority of males infertile as associated with absent vas deferens. Females, while fertile, may struggle to conceive or carry pregnancy unless in good health
46
What is primary ciliary dyskinesia?
Defective epithelial cilia lining airways: movement either not in unison or is static (the arrangement of interlocking columns of protein within the cilia become disrupted preventing uniform movement): mucous accumulation & poor airway clearance. If untreated, can lead to recurrent infections, bronchiectasis & eventual respiratory failure.
47
What are the clinical features of primary ciliary dyskinesia?
- Recurrent chest infections
- Persistent wet cough
- Unexplained neonatal respiratory distress (common clinical feature in neonates)
- Conductive hearing defects
- Congested auditory canal: grommet insertion can be devastating as can result in constant foul smelling ear discharge (cilia clearance affected as in chest)
- Sinusitis
- Dextrocardia
Cilia beat patterns & directions dictate orientation of the developing organs: abnormalities of the heart orientation or abdominal organs can occur. Any child with dextrocardia should be investigated for PCD.
48
What investigations should be done for primary ciliary dyskinesia?
- Nasal nitric oxide: sensitive but pathophysiology not fully understood
- Abnormal direction or static cilia is diagnostic
Research ongoing as to genetic cause: several genes associated with cilia structure abnormalities
49
Management and prognosis of primary ciliary dyskinesia?
Management: airway clearance techniques (physiotherapy, inhaled therapies), low threshold for treating suspected chest infection with Abx, sinus rinse to treat ENT symptoms which can be quite debilitating
Prognosis: mild cases result in normal life span, however, severe untreated disease will result in eventual respiratory failure.
50
What is pneumonia? What causes it?
Inflammatory condition of small airways
Bacterial
1. Streptococcus pneumoniae
2. Staphylococcus aureus
3. Haemophilus influenzae
4. Mycoplasma
Viral
1. Adenovirus
2. Rhinovirus
3. RSV
51
How does the presentation of pneumonia vary depending on virus vs bacteria?
Bacterial: all age groups, fever >38.5, RR >50, minimal recession, no wheeze, clinical and radiological signs of consolidation rather than collapse (more focal signs)
Viral: more common in infants & young children, fever <38.5, RR normal or raised, marked recession & hyperinflation (loss of liver dullness on chest percussion). Radiograph: hyperinflation and in 25% of cases, patchy collapse / consolidation.
Still very difficult to differentiate e.g. while focal signs more common with bacteria, can also get generalised CXR changes with other bacteria e.g. mycoplasma.
52
What is the impact of pneumonia worldwide?
Leading cause of childhood death (most common cause in low income counties).
Improving immunisation program against pneumococcus: PCV -13 against 13 serotypes of streptococcus pneumoniae (~100 exist, most common ones are now covered).
53
What are the features of mild-moderate pneumonia?
Infant: Temp >38.5°, RR <50 with mild recession, feeding well
Older child: temp >38.5°, RR <50 with mild breathlessness, no vomiting
54
What are the symptoms of pneumonia?
Pyrexia: main way to differentiate from asthma - absence of pyrexia on background of significant consolidation (CXR) is suspicious: consider TB & malignancy
Cough: may be associated with vomiting in younger children & sputum production in older children. Can be episodic or constant.
Tachypnoea & respiratory distress: accessory muscles, tachypnoea, tracheal tug, SC & intercostal recession.
Infants may have apnoeas due to poorer central respiratory control.
With severe enough hypoxia, any child may be cyanotic.
Grunting (forced expiration against a closed glottis) another sign of distress.
Poor feeding: suggestive of poor health in very young child – must take seriously (inability to take feeds due to coughing or general exhaustion is a common reason for hospital admission) – vomiting that can be associated with pneumonia can result in poor oral intake & dehydration
Abdominal pain: pleuritic pain can present as abdominal pain in some children, often with very few signs of respiratory distress
55
What clinical examination findings are suggestive of pneumonia?
Reduced air entry
Bronchial breathing
Dull percussive note
Stony dull suggests effusion which is a complication of pneumonia: concerning if developing empyema
Crepitations: inflamed tissue rubbing against each-other, or the opening & collapsing of small airways under the pressures of inspiration and expiration due to secretions.
Asymmetrical chest wall movement
Increased tactile vocal fremitus
Increased whispering pectoriloquy
Note: crackles suggest improving air entry
56
Apart from bacterial and viral infections, what other causes can present as pneumonia?
Mycoplasma (tuberculous and non-tuberculous) should be considered in high risk areas & populations.
Underlying immune problems can present as repeated infections (any child post-immunisation who acquires pneumonia secondary to pathogen covered by the vaccination should be suspect).
Long-standing Hx of coughing & respiratory distress when feeding could suggest pneumonia is secondary to aspiration.
57
Investigations for pneumonia?
None if well child with CAP (clear diagnosis), however, if moderate-severe case, or diagnostic doubt:
Bloods, blood culture, legionella urinary antigen test, sputum culture (best indication of pathogen), urinary pneumococcal antigen (not done at all centres, shows if exposed to pneumococcus but not necessarily cause of acute infection), CXR, chest USS
More severe cases:
• CT may be useful to exclude malignancy
* Bronchoscopy for induced sputum samples, look for any suspected malignancy or exclude inhaled foreign body in if recurrent infection
* Baseline immune function: immunoglobulin levels, functional antibody responses to immunisations, lymphocyte subsets may be tested if there are concerns about an underlying immunodeficiency (concerns may arise due to unusual infecting pathogens or unusually frequent or severe infections)
* Pleural aspiration: if pleural effusion, may be done therapeutically to drain the effusion or diagnostically to identify the cause of the effusion
58
What blood tests might be done in pneumonia?
Blood: WCC (↑ + may have neutrophilia, particularly if bacterial, normal WCC with consolidation or effusion may suggest malignancy), CRP (often doesn't peak until 24 hours so don't rely on this if child presents early – in very severe infection, CRP may not rise as synthetic protein cannot be produced if liver fails, empyema often drops proteins & spikes CRP up to ~300), U&Es, Albumin
Blood culture: important if unwell febrile child – septicaemia: viral serology, specific tests for legionella (urinary antigen test) and mycoplasma (blood PCR)
59
What are differentials for pneumonia?
Differentials: children can be breathless for many reasons, however, infection most likely cause in younger children. Without signs of infection or inflammation: consider undiagnosed cardiac lesion. Respiratory distress and consolidation without supporting inflammation is suggestive of malignancy – (both rare in children).
60
What imaging might be done in pneumonia?
CXR: focal consolidation or bilateral changes – always pay attention to cardiac border behind the heart!
Chest USS: if CXR suggests effusion then USS confirms presence, measures depth and describes whether it contains debris or is loculated: collections deeper than 2cm may require draining depending on context
o Differentiates pleural fluid from consolidated lung
o Demonstrates fibrinous strands within fluid, assesses loculation of fluid (signs of empyema), estimates size of effusion & guides chest drain placement
o Cannot accurately differentiate between an exudate & pus in the pleural cavity
61
What sputum culture tests may be done in pneumonia?
Best indication of pathogen
Bacterial + mycobacterial culture (can take up to 8 weeks) or viral PCR can direct treatment (myco + viral usually only for severe or unusual cases). If difficult (e.g. younger children), sputum induction using hypertonic NaCl nebuliser or rarely bronchoscopy for lavage samples
62
Prognosis and complications of pneumonia?
Prognosis: most make full recovery, however, repeated infections can lead to bronchiectasis (scarring resulting in permanent enlargement of the airways – best seen on CT). Such patients are vulnerable to long-term repeated infections.
Complications: parapneumonic effusions, empyema, lung abscesses, septicaemia, respiratory failure & dehydration
63
Management of pneumonia (broadly speaking)?
* Antibiotics: difficult to differentiate bacterial and viral, oral vs IV controversial and variability in clinical practice (generally move in preference for oral Abx where poss)
* Supportive measures: oxygen requirements (>92%), hydration & nutrition support. If background of chronic disease (e.g. CF, immunodeficiency, bronchiectasis) – often treated more aggressively for the same presentation as more vulnerable to opportunistic infections & may decompensate more rapidly due to poorer baseline respiratory function
o Physiotherapy if collapse
• Chest drain + urokinase (breaks down fibrinous strands / septi in empyema)
Note: in more recent years empyema management becoming more complex – previously cleared with urokinase, now seeing more complex parenchymal involvement > lung abcesses, pneumatoceles, bronchopleural fistulas – most likely caused by Group A Strep
64
Management of pneumonia (broadly speaking)?
o Antibiotics: difficult to differentiate bacterial and viral, oral vs IV controversial and variability in clinical practice (generally move in preference for oral Abx where poss)
o Supportive measures: oxygen requirements (>92%), hydration & nutrition support. If background of chronic disease (e.g. CF, immunodeficiency, bronchiectasis) – often treated more aggressively for the same presentation as more vulnerable to opportunistic infections & may decompensate more rapidly due to poorer baseline respiratory function
o Physiotherapy if collapse
o Chest drain + urokinase (breaks down fibrinous strands / septi in empyema)
Note: in more recent years empyema management becoming more complex – previously cleared with urokinase, now seeing more complex parenchymal involvement > lung abcesses, pneumatoceles, bronchopleural fistulas – most likely caused by Group A Strep
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What Abx therapy is given in pneumonia?
Difficult to differentiate bacterial & viral – oral vs IV Abx is controversial & variability in clinical practice (generally a move in preference for oral Abx where possible).
IV given in cases of suspected septicaemia, complications, severe HAP & those unable to take oral medications.
• Oral Abx:
Younger children with CAP: penicillin (e.g. amoxicillin) usually first line. Older children (mycoplasma more common): macrolide (e.g. erythromycin / clarithromycin) may be more appropriate on its own or in conjunction with a penicillin
• IV antibiotics:
Suspected septicaemia, complications, severe HAP + those unable to take oral medications: first-line usually penicillin or 2nd/3rd generation cephalosporin with consideration of additional macrolide cover for atypical infection (e.g. mycoplasma)
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What is bronchiectasis? What are common causes?
Abnormal fixed dilatation of airways (usually result of persistent and/or recurrent infections). Breakdown of airway walls, due to persistent inflammation, reduces ability to clear mucus and secretions & increases risk of infection
Common causes:
• Chronic conditions e.g. CF, PCD, immunodeficiency
• Acute infections e.g. measles
• Obstruction e.g. foreign body tumour
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What are the features of bronchiectasis?
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Features:
• Recurrent wet cough due to poor airway clearance
• Episodes of haemoptysis & wheeze
• Propensity to frequent infections
• Clubbing
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What investigations are done for bronchiectasis?
* CT: gold standard (distribution, extent & severity)
* CXR: bronchial wall thickening
* Sputum culture: not needed for diagnosis but useful for identifying persistent microbiology: for younger children unable to produce samples, induction with nebulised hypertonic NaCl or bronchoscopy may benefit
Lung function is poor indicator of an exacerbation: sputum volume and colour more telling.
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Prognosis and management of bronchiectasis?
Management
• Physiotherapy
• Inhaled therapies
• Low threshold for Abx in suspected infection
Prognosis: child with mild bronchiectasis has normal life expectancy, however, severe untreated disease will eventually cause respiratory failure
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What is a pneumothroax? Most common cause?
Air collection in pleural space due to underlying pathology (CF, asthma, severe infection) or trauma.
Most common cause: burst lung cyst. Tall, slim individuals more at risk (in these cases consider undiagnosed predisposing condition such as Marfan syndrome).
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Features of a pneumothorax?
Simple will be asymptomatic, however:
* Auscultation: absent breath sounds & reduced air entry on affected side
* Hyper-resonant percussion note
* If tension is developing: signs of respiratory distress along & tracheal deviation away from the affected side (emergency, leads to hypoxia)
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Management of a pneumothorax?
* Conservative: uncomplicated cases may resolve spontaneously and require no active management – O₂ helpful even in non-hypoxic patient as nitrogen (from air in the pleural space) will diffuse into the lungs (filled with 100% O₂) down its conc. gradient
* Needle aspiration: necessary in tension cases followed by chest drain insertion: aspirate from mid-clavicular 2nd intercostal space in mid-clavicular line
* Chest drain insertion: prevents escaping air compromising the patient while underlying defect repairs: mid-axillary 5th intercostal space
* Surgical: recurrent or complicated cases may require intervention such as pleurodesis where a substance is injected into the pleural space to encourage adhesion of the pleural layers
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Epidemiology of tuberculosis?
>9 million new cases/year, disproportionate in disadvantaged, malnourished & crowded areas. Highest rates are in SE Asia, Africa & Western Pacific. Rates thought to have increased due to emigration & HIV epidemic.
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What types of TB are there (clinically?)
Active (symptoms & contagious disease) or latent (present but suppressed by immune system). Most people infected with M. tuberculosis do not develop active disease (latent only), more likely in immunocompromised patients e.g. HIV-infected individuals.
Primary TB: when infection first occurs
Miliary TB: when primary infection is not adequately contained (severe disease from haematogenous spread)
Secondary TB: reactivation of latent TB (which may be precipitated by impaired immunity e.g. HIV, malnutrition, immunosuppressants).
Droplet transmission from active disease > commonly settle in distal respiratory bronchioles or alveoli > phagocytosed > transported to regional lymph nodes then other organs. If bacilli overcome immune defences: transition from infection to active TB. Primary active TB occurs when mediastinal nodes enlarge causing cavitation & spread to adjacent bronchi.
- Lymphohaematogenous dissemination can result in miliary TB or TB meningitis (bacilli can remain dormant in the apical posterior areas of the lung for several months or years) - later progression of disease > miliary TB.
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What causes tuberculosis (pathogens)?
Mycobacteria are acid-fast bacilli, slow-growing & aerobic.
1. Mycobacterium tuberculosis (most common)
2. M. bovis
3. M. africanum
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Which children should be considered for TB? What are the symptoms?
Children with pneumonia, pleural effusion or cavitating mass not responding to antibiotics
Features: fever, faltered growth, haemoptysis, night sweats, weight loss, lethargy, lymphadenopathy
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Investigations for TB?
* Tuberculin skin test (TST): intradermal injection of tuberculin purified protein derivative: inner surface of forearm. Causes palpable raised hardened area, measure size in mm within 48-72 hours. Positive test if >5mm.
* CXR: mediastinal enlargement, cavitating primary disease, lobar pneumonia
* Sputum culture: testing for acid fast bacilli using Ziehl-Neelsen stain (initial screen) before culture results (up to 8 weeks by conventional methods). Sputum culture can be performed in older children relatively easily, but if <6 years: early morning gastric aspirates may be required (contains swallowed respiratory secretions from night before). bronchial lavage may be required.
*Rapid tuberculosis diagnostic tests increasingly recognised as gold standard: based on nucleic acid amplification & unlike sputum cultures can give results within few hours rather than weeks
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Management of TB?
Both latent & active TB should be treated, aim to achieve sterilisation of the TB lesion in shortest time possible. Combination therapy at least 6 months for active TB.
o Rifampicin: inhibits bacterial RNA synthesis (RNA polymerase) - side effects: hepatitis
o Isoniazid: inhibits growth of cell wall - side effects: hepatitis, pancytopenia, peripheral neuropathy
o Pyrizinamide: inhibits growth of cell wall- side effects: joint pain, hepatitis
o Ethambutol: inhibits growth of the bacterial cell wall- side effects: optic neuritis & hepatitis
o Streptomycin: aminoglycoside antibiotic- side effects: neuropathy, nephropathy
Multi-drug resistant (MDR) TB: if resistant to at least Isoniazid & Rifampicin: increasing problem worldwide.
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Prevention of TB?
BCG vaccination to all babies born in areas with high rates or into a household with possible contacts.
Recent contact with active TB should be treated despite normal TST (particularly <5 years or with HIV). Public health should also be notified.
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Complications and prognosis of TB?
Respiratory Complications: effusions, collapse, pneumothorax, bronchiectasis (note : other systems e.g. small bowel, spleen, spine & heart can be affected)
Miliary TB & TB meningitis are most deadly complications of primary TB
Prognosis: full resolution expected in non-MDR and non-immunocompromised individuals (secondary TB can occur but in high endemic areas – recurrent disease more likely to be due to reinfection)
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What is Whooping cough?
Caused by Bordetella Pertussis & classically has incubation of 10-14 days. Children infectious for ~3 weeks after onset of classical symptoms. Most cases in UK or other countries where vaccination uptake is good are in infants <2 months or in unvaccinated children.
1. Catarrhal phase: build-up of mucus & fever
2. Paroxysmal cough (the ‘100 days’ cough): persistent series of coughing until large inhalation against inflamed upper airway (‘whoop’) – this phase can be very prolonged & result in vomiting and apnoea in infants
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What investigations for whooping cough?
Postnasal swabs: can be used to culture the bacteria or for direct immunofluorescence testing, only useful in the first few weeks of illness (after, serology for antibodies against pertussis may be used)
FBC: elevated WCC with high lymphocytosis (up to 80% of total white count)
Imaging will be invariably normal and is not indicated unless another alternative or concurrent diagnosis is suspected.
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How can whooping cough be prevented?
* Mothers vaccinated antenatally
* Pertussis immunisation at 2, 3 and 4 months, followed by preschool booster: protects 70% of patients and ameliorates illness in 30% (vaccinated can still develop the illness)
Reduction in the uptake of the pertussis vaccine in the UK and elsewhere, increasing the risk of the disease both for the child and for the community
Children <1 year should be offered Abx prophylaxis if they are a close contact (generally living in the same household) of someone diagnosed with pertussis.
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How is whooping cough managed?
Most cases can be treated at home with good education & reassurance, particularly when explaining to parents that the cough can be present for a long time
* low threshold for admitting children <6 months
* supportive oxygen therapy when coughing paroxysm occurs may be required to avoid hypoxia
Notifiable disease & children with suspected or confirmed diagnosis should stay off school / nursery for 5 days after starting antibiotics, or 21 days from the onset of cough (whichever is sooner). Contact with young children should be avoided particularly if they have not had their primary vaccination.
Children <1 year should be offered Abx prophylaxis if they are a close contact (generally living in the same household) of someone diagnosed with pertussis.
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Complications of whooping cough?
in severe cases the paroxysmal cough can result in sub-conjunctival haemorrhages, rib fractures, pneumothorax, hernia, post-cough fainting & even IVH or hypoxic brain injury.
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What is croup? What are the features?
Acute laryngotracheobronchitis
Most common cause: parainfluenza virus. Typically 1-2 years (rare <5), onset 1-2 days following URTI
- Barking cough (worse at night)
- Temp <38.5 (beware if very high fever – have they got trachitis, epiglottitis?)
- Hoarseness
- Coryzal symptoms
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How is croup managed?
Keep child as calm as possible + do not attempt throat exam (if upset: gets worse + can cause laryngospasm).
Stridor when resting & relaxed: criteria to admit.
Treatment dependent on croup score
- Oxygen and hydration
- Oral dexamethasone (preferred to prednisolone as longer acting)
- Nebulised budesonide
- Nebulised adrenaline (may need intensive care if adrenaline starting to wear off)
- Intubation (not very common)
CKS suggest admitting any child with moderate or severe croup. Other features prompting admission:
• <6 months age
• Known upper airway abnormalities (e.g. laryngomalacia, Down’s syndrome)
• Uncertainty about diagnosis (important differentials include acute epiglottitis, bacterial tracheitis, peritonsillar abscess & foreign body inhalation)
Note: CKS recommend that single dose 0.15mg/kg dexamethasone given to all children regardless of severity (high flow oxygen and nebulised adrenaline are emergency treatments)
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What are the features of MILD croup?
Occasional barking cough
No audible stridor at rest
No or mild suprasternal and/or intercostal recession
Child is happy and able to eat / drink / play
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What are the features of MODERATE croup?
Frequent barking cough
Easily audible stridor at rest
Suprasternal and sternal wall retraction at rest
No or little distress or agitation
Can be placated and interested in surroundings
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What are the features of SEVERE croup?
Frequent barking cough
Prominent inspiratory + occasionally expiratory stridor at rest
Marked sternal wall retractions
Significant distress and agitation, or lethargy or restlessness (sign of hypoxaemia)
Tachycardia occurs with more severe obstructive symptoms and hypoxaemia
