Paeds Resp Flashcards
What type of infection is pneumonia (URTI or LRTI)
lower respiratory tract infection
pneumonia- pathology
1- microbe manages to get past the protective mechanisms of the respiratory system (coughing, mucociliary escalator and alveolar macrophages) –> microbe multiplies and crosses from the airways to the lung tissue
2- tissue fills with white blood cells, proteins, fluids and RBCs (if capillary gets damaged) –> inflammatory response leads to fluid accumulation in the lungs
3- Many different microbes can cause pneumonia- these microbes can be acquired in different ways too
most common causative organisms of pneumonia in newborns
Group B strep most common, but also gram negative enterococci and bacilli (klebsiella, pseudomonas, pseudomonas)
most common causative organisms of pneumonia in infants and young children
RSV= most common, but also common are strep pneumonia/ H influenzae/ Bordatella pertussis/ Chlamydia trachomatis. Staph aureus is an infrequent but serious cause
most common causative organisms of pneumonia in children over 5 years
Mycoplasma pneumoniae, strep pneumoniae, chlamydia pneumoniae
which organism should be considered as a potential cause of pneumonia at all ages
mycobacterium tuberculosis
presentation of pneumonia in children
- usually preceded by an URTI, followed by fever, cough and rapid breathing
- lethargy, poor feeding
- localised chest/ abdominal or neck pain is a feature of pleural irritation and suggests bacterial infection
clinical features of pneumonia in children may include
- tachypnoea
- nasal flaring
- chest indrawing
- increased respiratory rate (most sensitive clinical sign)
- may have end-inspiratory crackles
- reduced oxygen saturation
tests for diagnosing pneumonia in children
- CXR confirms diagnosis but cannot reliably differentiate between bacterial and viral pneumonia. In a small proportion of children the pneumonia may be associated with pleural effusion where there may be blunting of the costophrenic angle on the CXR- some of these effusions may develop into empyema and fibrin strands may form, leading to septations
- in younger children a nasopharyngeal aspirate may identify viral causes. Blood tests are generally unhelpful in differentiating between viral and bacterial causes
criteria indicating hospital admission for pneumonia in children
- oxygen saturation <92%
- recurrent apnoea
- grunting
- inability to maintain inadequate fluid/feed intake
supportive care which should be provided to children with pneumonia
- oxygen if hypoxia
- analgesia if there is pain
- IV fluids should be given if necessary to correct dehydration and maintain adequate hydration and sodium balance
choice of antibiotics for children with pneumonia:
1- newborns
2- older infants
3- children over 5
1- newborns require broad-spectrum IV antibiotics e.g. gentamicin or cefotaxime
2- older infants can normally be managed with oral amoxicillin UNLESS it is pneumonia due to mycoplasma pneumonia (this should be treated with a macrolide). Broad spectrum antibiotics such as co-amoxiclav are reserved for complicated/unresponsive pneumonia
3- children over 5: amoxicillin or an oral macrolide (e.g. erythromycin, clarithromycin, azithromycin). No advantage to giving IV rather than orally if there is mild/moderate pneumonia
persistent fever despite 48hrs of antibiotics in children with pneumonia suggests…
a pleural collection which requires drainage- should be done with ultrasound guidance
characteristic feature of croup
barking cough
85% of laryngotracheal infections in children are
viral croup
most common causes of croup in children
parainfluenza= most common cause, other causes include rhinovirus, RSV and influenza
ages when croup is most common in kids
usually occurs between 6 months to 6 years of age, peak incidence in 2nd year of life
clinical features of croup
typically begins with coryza (catarrhal inflammation of mucus membranes in the nose) and fever followed by:
- hoarseness due to inflammation of vocal cords
- barking cough due to tracheal oedema and collapse
- harsh stridor and chest recession (when upper airway obstruction is mild, stridor and chest recession disappear when child is at rest and child can usually be managed at home)
- symptoms often start and are worse at night
investigations for croup
normally clinical diagnosis but CXR can be helpful:
- PA view shows subglottic narrowing (‘steeple sign’)
first line therapy for croup causing chest recession at rest
oral dexamethasone, prednisolone or nebulised steroids (budesonide)
NICE: all children should recieve a single dose of oral dexamethasone (0.15mg/kg), pred is the alternative if dexamethasone is not available.
- High flow oxygen and nebulised adrenaline can be used as emergency treatment
when should children with croup be admitted
- if they meet the criteria for moderate or severe croup
- <6 months of age
- known uppr airway abnormalities (e.g laryngomalacia or down’s syndrome)
- uncertainty about diagnosis (important differentials include acute epiglottitis. bacterial tracheitis, peritonsillar abscess and foreign body inhalation)
mild croup criteria
- occasional barking cough
- no audible stridor at rest
- no/mild suprasternal and/or intercostal recession
- child is happy and prepared to eat, drink and play
moderate croup criteria
- frequent barking cough
- easily audible stridor at rest
- suprasternal and sternal wall retraction at rest
- no or little distress/agitation
- children can be placated and is interested in surroundings
severe croup criteria
- frequent barking cough
- prominent inspiratory (and occasionally expiratory) stridor at rest
- marked sternal well recession
- significant distress and agitation, or lethargy or restlessness (a sign of hypoxaemia)
- tachycardia occurs with more severe obstructive symptoms and hypoxaemia
why is acute epiglottitis an acute emergency
it can be life threatening due to the high risk of respiratory obstruction caused by the intense swelling of the epiglottis
causative organism of acute epiglottitis
Hib (H. influenza type B)
clinical features of acute epiglottitis in children
- high fever in a very ill, toxic-looking child
- intensely painful throat which prevents the child from speaking/swallowing + saliva drools down the chin
- soft inspiratory stridor + rapidly increasing respiratory difficulty over hours
- the child sitting immobile, upright with an open mouth to optimise the airway
- “tripod position”- patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position
how to differentiate between viral croup and acute epiglottitis
there is a cough with croup but minimal/absent in acute epiglottitis
what must you NOT do in children with suspected acute epiglottitis
attempt to lie the child down or examine the throat with a spatula or perform a lateral neck XR to identify the swollen epiglottitis and surrounding tissues. This is because they can precipitate total airway obstruction and death
investigations/diagnosis of acute epiglottitis
- diagnosis usually by direct visualisation
- X rays may be done- lateral view shows ‘thumb sign’
management in acute epiglottitis
- emergency airway support, may require endotracheal intubation
- oxygen
- IV antibiotics (usually ceftriaxone)
most common lower respiratory disease in the first year of life
bronchiolitis- approx 1 in 3 infants will develop clinical bronchiolitis and 2-3% will require hospitalisation
requirement of bronchiolitis diagnosis
coryzal prodrome followed by persistent cough AND:
- tachypnoea or chest recession (or both) AND
- either wheeze or crackles on chest auscultation
- fever (around 30% of the time) and poor feeding
- younger babies (under 6wks) may present with apnoea without other clinical signs
Management of bronchiolitis
- oxygen if child’s oxygen saturation is less than 92%
- CPAP if children have impending respiratory failure
- upper airway suctioning in children with apnoea (even if there are no obvious upper airway secretions) and consider it in children with respiratory distress or feeding difficulties
- give fluids nasogastrically to children with bronchiolitis if they cannot take enough fluid by mouth, and IV if they cannot tolerate it
- capillary bloods
pathophysiology of asthma
genetic predisposition/atopy/environmental figures trigger;
1- Bronchial inflammation- leads to oedema, excessive mucus production, infiltration (eosinophils, mast cells, neutrophils, lymphocytes)
2- bronchial hyperresponsiveness- exaggerated twitchiness to inhaled stimuli
3- airway narrowing- reversible airflow obstruction (e.g. peak flow variability)
4- Symptoms: wheeze, cough, breathlessness, chest tightness
clinical features of Asthma
- Asthma should be suspected in any child with wheezing on more than one occasion- confirmed through auscultation
- more common in children with personal/family history of atopy
- symptoms worse at night and in the early morning
- nonviral triggers
- interval symptoms- symptoms between acute exacerbations
- positive response to asthma therapy
possible examination findings in childhood asthma
- hyperinflation of the chest
- generalised polyphonic expiratory wheeze with prolonged expiratory phase
What are Harrison’s sulci?
depressions at base of thorax associated with muscular insertion of the diaphragm, caused in onset of asthma in early childhood. Associated with chronic obstructive airway disease such as asthma from chronic increased work of breathing.
presence of wet cough, sputum production, finger clubbing or poor growth in children suggests
a condition characterised by chronic infection such as cystic fibrosis or bronchiectasis
diagnosing asthma in children
- clinical diagnosis if under 5 years old- treat symptoms
- If 5 or over, offer spirometry (FEV1:FVC ratio) and check for bronchodilator reversibility
- If 5-16, do the above and then if uncertain test fraction exhaled nitric oxide (greater than 35ppm is suggestive of asthma)
Management algorithm of Asthma in children (5-16)
1- SABA- used for newly diagnosed asthma
2- SABA+ paed low dose ICS (e.g. beclamethasone)- used when SABA alone does not control asthma OR if newly diagnosed with 3 or more symptomatic episodes / night time waking
3- SABA + paed low dose ICS + LTRA (e.g. montelukast)
4- SABA+ paed low dose ICS + LABA (e.g. salmeterol) - unlike adult, stop LTRA at this point if it hasn’t helped
5- SABA + switch ICS/LABA for a maintenance and reliever therapy (MART) that includes a paediatric low-dose ICS
6- SABA + paediatric moderate dose ICS MART OR consider changing back to a fixed-dose of a moderate-dose ICS and a separate LABA
7- SABA and one of the following options:
- increase ICS to paediatric high-dose, either as part of a fixed-dose regime or as a MART
- a trial of an additional drug (for example theophylline)
- seeking advice from a healthcare professional with expertise in asthma
Management algorithm of Asthma in children aged less than 5 years
1- SABA for newly diagnosed asthma
2- SABA + 8 week trial of paediatric moderate-dose inhaled corticosteroid; after 8 weeks, stop ICS and review: if symptoms stopped and reoccurred within 4 weeks, restart ICS at low-dose, if symptoms stopped and reoccurred beyond 4 weeks after stopping ICS treatment, repeat the 8-week trial of a paediatric moderate dose of ICS
3- SABA + paediatric low dose ICS + LTRA
4- stop LTRA and refer to paediatric asthma specialist
what are the paediatric doses of inhaled corticosteroids?
- <= 200 micrograms budesonide or equivalent = paediatric low dose
- 200 micrograms - 400 micrograms budesonide or equivalent = paediatric moderate dose
- > 400 micrograms budesonide or equivalent= paediatric high dose.
what does a normal pCO2 indicate in an asthma attack, and why?
Initially compensation occurs and hyperventilation causes the PCO2 to decrease. When further air trapping leads to decreased lung compliance and increased work of breathing, the PCO2 will begin to increase. Thus, a “normal” pCO2 in a wheezing patient is a sign of a moderately severe attack.
acute asthma criteria for admission
admission is required if after high-dose inhaled bronchodilator therapy, they
- have not responded adequately clinically i.e. if there is persisting breathlessness or tachypnoea
- Are becoming exhausted
- Still have marked reduction in their predicted (or usual best) peak flow rate or FEV1 (<50%)
- Have a reduced oxygen saturation (<92% in air)
life-threatening asthma signs
- silent chest, cyanosis
- poor respiratory effort
- exhaustion
- arrhythmia, hypotension
- altered consciousness
- agitation, confusion
- peak flow less than 33% (best)
- oxygen saturation <92%
life threatening acute asthma treatment
1- Short-acting B2 agonist nebulised (2.5mg salbutamol in <8yrs, 5mg in >8yrs), assess response continuously and repeat as required (back to back)
2- Oral prednisolone or IV hydrocortisone
3- Nebulised ipratropium
4- Consider IV B2 agonist (salbutamol) or aminophylline or magnesium
5-Discuss with PICU
Severe acute asthma signs
- too breathless to talk
- oxygen sat <92% for <12 year olds
- peak flow 33-50%
- resp rate:
• Greater than 40 breaths/min for 2-5yrs
• Greater than 30 breaths/min for 5-12yrs
• Greater than 25 breaths/min for 12-18yrs - Heart rate:
• Greater than 140 beats/min for 2-5yrs
• Greater than 125 beats/min for 5-12yrs
• Greater than 110 beats/min for 12-18yrs
Treatment severe acute asthma
- Short-acting B2 agonist via spacer, 10 puffs or nebulised (2.5mg salbutamol in <8yrs, 5mg in >8yrs)
- Oral prednisolone or IV hydrocortisone
- Consider:
- Inhaled ipratropium
- IV B2 agonist (salbutamol) or aminophylline or magnesium
signs moderate asthma
• Able to talk
• Oxygen saturation >92%
• Peak flow >50% [best]
• Resp rate:
• Less than or equal to 40 breaths/min for 2-5yrs
• Less than or equal to 30 breaths/min for 5-12yrs
• Less than or equal to 25 breaths/min for 12-18yrs
• Heart rate:
• Less than or equal to 140 beats/min for 2-5yrs
• Less than or equal to 120 beats/min for 5-12yrs
Less than or equal to 110 beats/min for 12-18 yrs
Treatment- moderate asthma
- Keep calm and reassure child and parents
- Short-acting B2 agonist via spacer (with face mask for those under 3), 2-4 puffs increasing by 2 puffs every 2 min to 10 puffs if required
- Oral prednisolone 1-2 mg/kg, max 40mg
- Monitor response for 15-30mins
causes of acute wheezing in children
1- asthma
2- viral episodic wheezing
3- atypical pneumonia (caused by mycoplasma, chlamydia or adenovirus)
4- foreign body inhalation- most likely to be in right main bronchus
5- anaphylaxis
is cystic fibrosis autosomal dominant or recessive
autosomal recessive
average life expectancy for someone with CF
40s for current newborns (previously 30s)
What causes CF
defective protein called CFTR - a cyclic AMP-dependent chloride channel found in the membrane of cells. This causes abnormal ion transport across epithelial cells causing multisystem dysfunction which results in effects such as
- reduction in airway surface liquid layer + consequent impaired ciliary function and retention of mucopurulent secretions
- chronic endobrachial infection with specific organisms e.g. pseudomonas aureginosa
- pancreatic ducts blocked by thick secretions
- meconium ileus (due to thick viscid meconium) in 10-20% of infants
- abnormal function of sweat glands results in excessive concentrations of sodium and chloride in the sweat
Where is the gene for CFTR located. What type of mutation occurs in CF?
chromosome 7. The most common mutation is ΔF508. This is a class II mutation (incorrect folding of the Endoplasmic reticulum, leads to reduction in CFTR mediated chloride transport)
how is pancreatic insufficiency diagnosed in CF
low faecal elastase
CF clinical features
- recurrent chest infections
- chronic infection, initially staph aureus and haemophilus influenzae and subsequently pseudomonas aureginosa and burkholderia specias –> results from viscid mucus in the smaller airways
- leads to damage to bronchial wall, bronchiectasis, abscess formation
- can cause diabetes mellitus due to pancreatic insufficiency
- meconium ileus may be present in newborns
CF diagnostic tests
- screening picks up raised IRT in newborn infants with CF during routine blood testing. These are then screened for common CF mutations; infants with 2 mutations have sweat test to confirm diagnosis (Cl 60-125 mmol/L)
- testing for gene abnormalities in CFTR protein
CF management
(1) Resp
(2) nutritional
- yearly review in specialist centre
- patients advised NOT to segregate with other CF patients as increased concern of cross-infection
RESP:
- daily (x2) physiotherapy to clear airways of secretions
- continuous prophylactic oral antibiotics- usually flucloxacillin
- macrolide antibiotic azithromycin given regularly
- nebulised DNAse or hypertonic saline may be helpful in decreasing viscosity of sputum and increase its clearance
(2) nutritional:
- pancreatic insufficiency is treated with oral pancreatic replacement therapy- enzymes taken with every meal
- high calorie and high fat diet is essential (gastrostomy often used)
- fat soluble vitamin supplements
how does CF affect fertility in patients
- males virtually always infertile due to absence of the vas deferens
- females have normal fertility
