Resp Flashcards
Features of asthma
Characterised by reversible and paroxysmal constriction of airways with airway occlusion by inflammatory exudate and late airway remodelling
Epidemiology of asthma
Commonest chronic condition in children
- 1 in 11
Peaks between 5 and 15 years of age
Pathophysiology of asthma
Multi-factorial disease
Susceptible individuals have an exaggerated response to various stimuli
Type 1 hypersensitivity
- driven by Th2 type T-cells
- allergens presented by dendritic cells
- cytokines released -> activation of humoral immune system
- increased proliferation of mast cells, eosinophils and dendritic cells
- leukotriene C4 and histamine
Trigger factor leads to airway inflammation
- hypersecretion of mucus
- airway muscle constriction
- swelling bronchial membranes
Leads to narrow breathing passages
Risk factors for asthma
Genetic factors - asthma/atopy in parents or siblings Environmental factors - low birth weight - parental smoking Viral bronchiolitis in early life Atopic dermatitis
Precipitating factors for asthma
Cold air and exercise
- drying of airways leads to cell shrinkage which triggers an inflammatory response
Atmospheric pollution
Drugs
- NSAIDs - shunt the arachidonic acid pathways towards the production of leukotrienes which are toxic to the epithelium
- beta-blockers - prevent bronchodilatory effect of catecholamines on airways
Exposure to allergens
Disease severity of asthma
Infrequent episodic wheezing - discrete episodes lasting a few days with no interval symptoms Frequent episodic wheeze - 2-6 weekly Persistent wheezing - most days and disturbed nights
Features of preschool wheeze
Wheezing very common in preschool children
- up to 50% have significant episode of wheeze by their 5th birthday
Most commonly caused by human rhinovirus or respiratory syncytial virus
Most outgrow their wheeze
Episodic viral wheeze - wheezing only in response to viral infection and no interval symptoms
Multiple trigger wheeze
- wheeze in response to viral infection but also to other triggers such as exposure to aeroallergens and exercise
Clinical features of asthma on examination
Signs - Expiratory wheeze - non-productive cough - worse at night - Dyspnoea and chest tightness - Features of atopy Signs - chronic - Hyperinflation of chest Signs - acute - Respiratory distress - Reduced chest expansion - Widespread polyphonic wheeze across the chest
Investigations for asthma
Spirometry - normal in between exacerbations - obstructive pattern (FEV1:FVC < 70%) - bronchodilator reversibility Peak Expiratory Flow Rate (PEFR) Bronchial provocation tests Exercise testing Skin prick testing Exhaled nitric oxide (ENO) - NO produced in bronchial epithelial cells - production increased in those with Th2-driven eosinophilic inflammation Baseline CXR
Management of asthma
Aim to achieve good symptom control
Stepwise approach
- step 1 = as required short-acting beta-2 agonist (salbutamol)
- step 2 = regular preventer therapy with inhaled corticosteriods
- step 3 = initial add on therapy
- long-acting beta-2 agonist = salmeterol/formoterol
- increase ICS dose
- leukotriene receptor antagonist = montelukast
- step 4 = increase dose of ICS
- step 5 = regular oral steroids and referral to respiratory paediatrician
General management points for asthma
Aerosol inhaler devices should always be used with a spacer device
Question compliance
LABA should not be prescribed as monotherapy - only in combination with ICS
Steroid equivalency
- fluticasone is 2x as potent as beclomethasone
All children should have an asthma management plan
Inhaler technique should be reviewed by asthma/practice nurse
Clinical features of acute asthma exacerbation
Mild - SaO2 > 92% - vocalising without difficulty - mild chest wall recession - moderate tachypnoea Moderate - SaO2 < 92% - breathlessness - moderate chess wall recession Severe - SpO2 < 92% - PEFR 33-50% predicted - RR > 30 (over 5), > 40(under5) - too breathless to talk/feed - HR > 125 (over 5), > 140 (under 5) - use of accessory muscles - audible wheeze Life threatening - SpO2 < 92% - PEFR < 33% predicted - silent chest - poor respiratory effort - altered consciousness - agitation/confusion - exhaustion - cyanosis
Immediate management of acute attack
Oxygen - high flow to maintain sats between 94-98% Bronchodilators - inhaled SABA - via nebuliser if severe - inhaler and spacer for mild/moderate Ipratropium bromide (anti-muscarinic) Corticosteroid - short course (3 days) - oral prednisolone - IV hydrocortisone if vomiting or too unwell
Second-line management of acute asthma attack
IV salbutamol
Magnesium sulphate
Safe-discharge criteria for asthma attack
Bronchodilators are taken as inhaler device with spacer at intervals of 4-hourly or more (e.g. 6 puffs salbutamol via spacer every 4 hours)
SaO2 >94% in air
Inhaler technique assessed/taught
Written asthma management plan given and explained to parents
GP should review the child 2 days after discharge
Define bronchiectasis
Abnormal dilation of airways with associated destruction of bronchial tissue
- reversible in children
- commonly occurs as a result of CF
Epidemiology bronchiectasis
Prevalence of non-CF bronchiectasis is 172/ million children
Pathophysiology of non-CF bronchiectasis
Inflammatory response to a severe infection leads to structural damage within bronchial walls -> dilation
- scaring reduces number of cilia
- predisposes to further infections
Causes of non-CF bronchiectasis
Post infectious - Streptococcus pneumonia - Staphylococcus aureus - Adenovirus - Measles - Influenza virus - Bordetella pertussis - Mycobacterium tuberculosis Immunodeficiency - Antibody defects: agammaglobulinaemia, common variable immune deficiency or IgA/IgG deficiency - HIV infection - Ataxia telangiectasia Primary Ciliary Dyskinesia (PCD) - autosomal recessive genetic defect - reduced efficacy or complete inaction of bronchial cilia Post-obstructive - foreign body aspiration Congenital syndromes - Young’s syndrome: A rare condition associated with bronchiectasis, reduced fertility and rhinosinusitis - Yellow-nail syndrome: Another rare syndrome associated with pleural effusions, lymphoedema and dystrophic nails - Bronchiectasis occurs in around 40% of patients
Clinical features of bronchiectasis
Purulent sputum expectoration Chest pain Wheeze Breathlessness on exertion Haemoptysis Recurrent or persistent infections of the lower respiratory tract Finger clubbing Inspiratory crackles Wheezing
Investigations for bronchiectasis
CXR
- bronchial wall thickening or airway dilation
HRCT = gold standard
- bronchial wall thickening
- diameter of bronchus larger than that of accompanying artery - signet ring sign
- visible peripheral bronchi
- bilateral upper lobe ≈ CF
- unilateral upper lobe ≈ post-TB infection
- focal ≈ foreign body inhalation
Bronchoscopy
- reserved for children who have evidence of focal bronchiectasis on CT
Lung function tests
- normal in mild disease
- obstructive or mixed in severe disease
Investigations to determine underlying cause in bronchiectasis
Chloride sweat test - exclude CF FBC + leukocyte differential Immunoglobulin panel - immunoglobulin deficiency Specific antibody level - pneumococcal or Hib Ciliary brush if bronchoscopy performed HIV test Microbiological assessment - Pseudomonas spp ≈ CF
Management of bronchiectasis
Chest physio - learn mucus clearance techniques Abx in exacerbations Bronchodilators in those with a wheeze Follow up and monitoring of symptoms and lung funtion
Common infective causes of bronchiectasis exacerbations
Haemophilus influenzae
Streptococcus pneumoniae
Moraxella catarrhalis
Complications of bronchiectasis
Recurrent infection Life-threatening haemoptysis Lung abscess Pneumothorax Poor growth and development
Define bronchiolitis
Viral infection of bronchioles - smallest air passages in the lungs
- commonly caused by respiratory syncytial virus
Epidemiology of bronchiolitis
Usually affects children under age of 2
1/3 develop in 1st year of life
Mainly occurs during winter and spring
- 75% caused by RSV
Pathophysiology of bronchiolitis
Infection of lower respiratory tract - cell necrosis - inflammation - oedema - increased mucus secretion Leads to - hyperinflation - increased airway resistance - atelectasis - ventilation-perfusion mismatch
Risk factors for bronchiolitis
Being breast fed for less than 2 months
Smoke exposure
Having siblings who attend nursery or school - increased risk of exposure to viruses
Chronic lung disease due to prematurity
Prematurity
Immunodeficiency
Congenital/acquired lung and cardiac disease
Clinical features of bronchiolitis
Increasing symptoms over 2-5 days Low-grade fever Nasal congestion Rhinorrhoea Cough Feeding difficulty Tachypnoea Grunting Nasal flaring Intercostal, subcostal or supraclavicular recessions Inspiratory crackles Expiratory wheeze Hyperinflated chest Cyanosis or pallor
Differential diagnosis of bronchiolitis
Pneumonia Croup Cystic fibrosis Heart failure – VERY IMPORTANT Bronchitis Asthma Viral wheeze
Investigations for bronchiolitis
Nasopharyngeal aspirate or throat swab – RSV rapid testing and viral cultures
Blood and urine culture if child is pyrexic
FBC
Blood gas (ABG) if severely unwell – this may detect respiratory failure and the need for respiratory support, but should not be done routinely
CXR (only if diagnostic uncertainty or atypical course)
- Hyperinflation
- Focal atelectasis
- Air trapping
- Flattened diaphragm
- Peribronchial cuffing
Management of bronchilitis
Most managed at home - fluids, good nutrition and temperature control Severe referred to hospital - oxygen and NG feeding Palivizumab offered to high risk infants - vaccine
Criteria for urgent hospital referral for management of bronchiolitis
Apnoea Poor feeding Child looks seriously unwell Severe respiratory distress eg. grunting, marked recessions, respiratory rate >70 Central cyanosis Oxygen sats < 94% Hospital referral considered if - resp rate > 60 - inadequate fluid intake - clinical dehydration
Management of bronchiolitis
Primary care
- conservatively managed at home with adequate hydration and anti-pyrexial medication
Secondary care
- supportive care - O2 and NG feeding
- nebulised saline and nebulised adrenaline
- bronchodilators, corticosteriods and abx have no effect
Vaccine
- palivizumab offered to high risk infants
Complications of bronchiolitis
Hypoxia
Dehydration
Fatigue
Respiratory failure
Persistent cough or wheeze - very common and parents should be counselled that their child may cough for several weeks
Bronchiolitis obliterans – airways become permanently damaged due to inflammation and fibrosis
Prognosis of bronchiolitis
Usually lasts 7-10 days
Cough up to 6 weeks
Pathophysiology of COVID-19
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)
Main transmission via respiratory droplets - coughing, sneezing and talking
Risk factors for severe illness from COVID-19
Solid organ transplant recipients Certain cancers/those undergoing therapy Severe respiratory conditions - cystic fibrosis - severe asthma Immunodeficiency disorders Those on long term immunosuppressive therapies
Clinical features of COVID-19
Fever Dry cough Headache Sore throat Myalgia SOB Diarrhoea N+V Coryza Abdo pain Low O2 sats Increased RR Subcostal/intercostal recession Tracheal tug Tachycardia Crackles on auscultation
Features of Paediatric Inflammatory Multisystem Syndrome
Associated with SARS-CoV-2 infection Toxic shock syndrome Atypical Kawasaki disease Blood parameters consistent with severe COVID-19 Coronavirus positive or negative
Severity of COVID-19
Mild - no pneumonia or mild pneumonia Severe - dyspnoea - oxygen sats < 93% - > 50% lung infiltrates within 24-48 hours Critical - resp failure - septic shock - multiple organ dysfunction/failure
Differential diagnosis of COVID-19
URTI LRTI Exacerbation of asthma Viral induced wheeze Exacerbation of asthma Allergy Gastroenteritis UTI Sepsis Kawasaki disease DM
Investigations for COVID-19
Viral throat and nose swab CXR - bilateral infiltrates Inflammatory markers - CRP and ESR elevated FBC - lymphopenia and neutrophilia Liver enzymes - elevated Lactate dehydrogenase - elevated D-dimer - raised
Management of COVID-19
Mild illness - supportive tx at home - isolate at home for 7 days from onset of symptoms - other members of household isolate for 14 days Hospital admission - O2 supplementation - Observation of fluid management - Continue regular meds - abx for secondary infection - inotropic support
Consider hospital admission for COVID-19
Increased work of breathing Ongoing fevers not controlled with antipyretics Signs of dehydration Increased lethargy Pale, blotchy, blue or grey skin
Complications of COVID-19
Acute respiratory distress syndrome (ARDS Sepsis PIMS-TS Multiorgan failure Arrhythmias Death
Define cystic fibrosis
Autosomal recessive disease
Caused by mutation in CF transmembrane conductance regulator gene (CFTR)
Epidemiology of cystic fibrosis
1 in 25 caucasian europeans are carriers
1 in 2500 live births have CF
Pathophysiology of cystic fibrosis
Autosomal recessive genetic mutation of CFTR gene on chromosome 7
Ordinarily functions to
- promote movement of chloride ions down concentration gradient
- out of cells and into secretions
- sweat cells reabsorb Cl- ions
- inhibit effect of Na channel
- Na moves intracellularly
Reduced Cl-, Na+ and H2P in secretions -> thicker more viscous mucus
Clinical features of CF
Neonates - meconium ileus - failure to thrive - prolonged neonatal jaundice Infancy - failure to thrive - recurrent chest infections - pancreatic insufficiency - steatorrhoea Childhood - rectal prolapse nasal polyps - sinusitis Adolescence - pancreatic insufficiency - DM - chronic lung disease - DIOS, gallstones, liver cirrhosis
Diagnosis of CF
Fitting clinical hx and positive chloride sweat test
Investigations for CF
CXR - hyperinflation, bronchial thickening
Chloride sweat test - annually if in receipt of CFTR potentiator/corrector therapy
Microbiological assessment - cough swab/sputum
Glucose tolerance test - teenage years beyond
Liver function test and coagulation
Bone profile
Lung function testing
Features of chloride sweat test
Measures electrolyte concentration in sweat
Sample collected by pilocarpine iontophoresis
Sweat chloride > 60mmol/l suggestive of CF
= 40-60 is borderline
Single test not sufficient to diagnose - second test or identification of genetic mutation
Management of CF
Patient and family education
- explain diagnosis and provide written information
Airway clearance and chest symptoms
- twice-daily physiotherapy to increase airway secretion
- Mucolytics
- DNase - inhaled and reduces viscosity of mucus by digesting DNA which is abundant in sputum
- hypertonic saline
Nourishment and exercise
- encourage physical activity
- pancreatic enzyme supplementation
- vitamin A, D and E
- monitor growth
- build-up milkshakes to supplement meals
Common causative organisms of airway infection in CF
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa
Treatment of airway infection in CF
2 weeks abx even if asymptomatic - high doses need to optimise sputum concentrations
Sputum culture preferable to cough swab
Prophylactic abx recommended in under 3s
Regular azithromycin reduce exacerbations and improve lung function
Management of pseudomonas aeruginosa infection in CF
Chronic infection a/w poorer lung function
Caused by environmental strain
Chronic infection leads to formation of biofilms
Tx with inhaled abx
Features of infection control in CF
Active segregation to reduce cross-infection
Pseudomonas naive patients attend different clinics to those with chronic infection
Admitted to side room
Respiratory complications of CF
Allergic bronchopulmonary aspergillosis
- immune response to presence of aspergillus spp.
- treated with prednisolone and itraconazole
Bronchiectasis
Haemoptysis
Pulmonary hypertension and right heart strain
Pneumothorax
Nasal polyps
GI complications of CF
Rectal prolapse Distal intestinal obstruction syndrome (DIOS) CF related liver disease - cholestasis - gallstones - liver cirrhosis
Endocrine complications of CF
CF related diabetes (CFRD)
- a/w rapid decline in lung function and disease progression
- weight loss, anorexia and fall in lung function
- ketoacidosis rare - not absolute lack of insulin
- screened for at yearly review
Delayed puberty
- average of 2 years
Other complications of CF
Arthritis
Reduced bone mineral density
Sub or infertility in later adolescence/adulthood
Define croup
Laryngotracheobronchitis
Viral infection that affects children
Can present as life-threatening airway compromise
Pathophysiology of croup
Commonly parainfluenza virus
- transmitted by resp droplets or through contamination of hand
Leads to tissue oedema and swelling
- limits airflow through upper respiratory tract
Epidemiology of croup
Affects children between 6 months and 3 years
Most prevalent late autumn
Slight male preponderance
Clinical features of croup
Hx of viral UTRI - progresses to barking cough Hoarse cry Inspiratory stridor Fever Respiratory distress - Increased RR, nasal flaring, tracheal tug, intercostal recession
Mx of croup
Admit if - < 6 months old - severe - resp distress - child looks very unwell O2 to main sats between 94 and 98% Single dose corticosteroids Nebulised adrenaline 1:1000 0.4ml/kg
Pathophysiology of LRTI/pneumonia
Inflammatory cascade triggered
- increased vascular permeability
- flow of plasma into alveoli
- reduced air space and consolidation
- airway narrowing due to tissue oedema
- increased mucus production
Common causative organisms of pneumonia
Bacterial - S.pneumoniae - H.influenzae - S. aureus - K. pneumoniae Viral - influenza A - RSV - VZV
Risk factors for LRTI
Exposure to infected children
Preterm birth
Cigarette smoke
Clinical features of LRTI
In neonates localised symptoms are rare - unwell febrile child
Symptoms of URTI precide illness
Cough
- purulent sputum
- commonly absent in younger children
Fever
Tachypnoea
REduced SpO2
Palpation - reduced chest expansion and dull percussion
Auscultation - coarse crackles, asymmetry of air entry, bronchial breath sounds or focal wheeze
Ix for LRTI
Identify causal organism - sputum culture taken - rarely comes back positive Bloods - raised WCC - blood culture CXR - consolidation
DDx of LRTI
Asthma Bronchiolitis Inhaled foreign body Cardiac disease GORD
Mx of LRTI
Simple analgesics and anti-pyretics
Antibiotics
- for mild disease - PO amoxicillin for 3 days
Admit children with sats < 92%, RR>70, increased HR, increased CRT or apnoea/grunting
Define obstructive sleep apnoea
Collapse of pharyngeal airway during sleep
Characterised by apnoea episodes during sleep
- person will stop breathing periodically for up to a few minutes
- usually reported by partner as patient unaware
Risk factors for obstructive sleep apnoea
Middle age Male Obesity Alcohol Smoking
Features of obstructive sleep apnoea
Apnoea episodes during sleep - reported by partner Snoring Morning headache Waking up unrefreshed from sleep Daytime sleepiness Concentration problems Reduced oxygen saturation during sleep Severe cases can cause - hypertension - heart failure - increased risk of MI and stroke
Mx of obstructive sleep apneoa
Referral to ENT specialist of specialist sleep clinic
- monitor O2 sats, HR, RR and breathing during sleep
Correct reversible risk factors
- stop drinking alcohol, smoking and lose weight
CPAP
- maintains patency of airway
Surgery
- restructuring of the soft palate and jaw
Define pneumothorax
Air gets into pleural space separating the lung from chest wall
- occur spontaneously or secondary to trauma, iatrogenic or lung pathology
Ix of pneumothorax
Erect CXR
- loss of lung marking
- measure size - horizontally from lung edge to inside of chest wall at level of hilum
CT Thorax - detect small pneumothorax that is too small for CXR
Mx of pneumothorax
If no SOB and < 2cm rim of air on the CXR = no treatment required - will spontaneously resolve
- follow up in 2-4 weeks
If SOB and/or there is a > 2cm rim of air CXR - aspiration and reassessment
- if aspiration fails twice it will require a chest drain
Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain
Pathophysiology of URTI
Mostly viral - rhinovirus or coronavirus
Inoculation occurs via
- child touching nose/mouth following direct contact with an infected surface
- inhalation of respiratory droplets
Viruses invade the mucosal surface, producing inflammatory response
Risk factors for URTI
School attendance
Second-hand smoking
Immunocompromised state
Clinical features of URTI
Nasal obstruction, sneezing and discharge
Sore throat
Headache
Non-productive cough - 1/3
Febrile
Feeding may be affected
Ears - otitis media with effusion
Nose - nasal mucosa erythematous and visible discharge
Throat - pharyngeal erythema and tonsillar swelling
Clear chest
Mx of URTI
Conservative and symptomatic
- encourage good oral hygiene
- inhalation of steam
- simple analgesics and anti-pyretics - begin with paracetamol then switch to ibuprofen if not sufficient
- over the counter cough syrup
- not abx
Define epiglottitis
Acute inflammation of epiglottis that can lead to serious airway obstruction
- now uncommon following Haemophilus influenzae type B (HIB) vaccination
Pathophysiology of epiglottitis
Bacterial infection caused by HIB, pneumococcus, group A beta-haemolytic streptococci and Pseudomonas
Epiglottis and surrounding tissue become acutely inflamed -> pharyngeal obstruction
Risk factors for epiglottitis
Most commonly seen before 8 years of age
Non-vaccination
Immunocompromise
Clinical features of epiglottitis
Early - drooling and dysphagia Late - dysphonia and dyspnoea Rapidly progressing sore throat should prompt consideration of this diagnosis Patient looks unwell Tripod position High temp Respiratory distress - nasal flaring, tracheal tug, raising shoulders, intercostal recession Inspiratory stridor
Ix for epiglottitis
Laryngoscopy - gold standard
Swabs of throat for MC&S
DDx of epiglottitis
Peritonsillar abscess Tonsillitis Retropharyngeal abscess Laryngotracheobronchitis Aspirated foreign body
Mx of epiglottitis
Secure airway - high flow O2 - nebulised adrenaline - intubation Treat infection - IV antibiotics Therapeutic adjuncts - IV steroid - reduce inflammation - IV maintenance fluids - patient NBM Recovery - extubation performed around 72 hours
Features of aspirated foreign body
Larger foreign bodies present with acute airway obstruction
Smaller FB move distal to the carnia
Pathophysiology of small aspirated foreign bodies
Typically food but can bee paper clips and coins
Carnia symmetrical < 15ys so FB may be found on either side
Consequences
- inflammation
- oedema
- ulceration
- infection
Epidemiology of aspirated foreign bodies
80% in under 3s
Neurological disorders increase likelihood
Clinical features of aspirated foreign bodies
Sudden episode of coughing, choking and crying
Unwitnessed and high index of suspicion required
Wheeze and dyspnoea
Fever, tachycardia, tachypnoea and low SaO2
Ix for aspirated foreign bodies
CXR
- radio-opaque in 10-20% of cases
- if radiolucent - atelectasis, unilateral hyperinflation or secondary pneumonia
Bronchoscopy - gold standard
Mx of aspirated foreign bodies
Bronchoscopy for retrieval of FB Manage choking Prevention - avoidance of easily aspirated foods - feed sitting upright - avoid playing whilst eating - keep small objects out of reach
Pathophysiology of whooping cough
Bordetella pertussis
Spread via respiratory droplets
Infection spreads to bronchi and bronchioles where exudate forms - compromise small airways -> atelectasis and pneumonia
Risk factors for whooping cough
Less than 6 months - incomplete immunity
Contact with infected children - respiratory droplet spread
Clinical features of whooping cough
Symptoms closely mimic those of URTI
Dry, hacking and prolonged cough
Inspiratory whoop - produced by forceful inspiration
Turn red in the face during episodes
Petechiae
Left with persistent cough that will last up to 3 months
Commonly afebrile
Ix for whooping cough
Pernasal swab
Increased WCC - high lymphocytes
CXR may show perihilar infiltrates and atelectasis
Mx of whooping cough
Supportive - good hydration, nutrition and oxygenation
Abx do not alter clinical course
