Respiration

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10 Respiration

History

Cough, snuffles, wheeze, breathlessness and stridor are the common respiratory symptoms in children. Wheeze is an expiratory whistling noise, but members of the public do not always understand the term. Even experienced doctors may on occasion get confused between expiratory wheeze and inspiratory stridor. Be careful, then, not to make assumptions. Ask about the nature of any cough as this is helpful in reaching a differential diagnosis. Upper airway coughs are often ‘barking’ in nature – like a seal rather than a dog. The cough associated with lower airway obstruction, such as bronchiolitis or asthma, is often described as ‘hacking’ or ‘dry’. A ‘fruity’ cough may indicate suppurative lung disease such as bronchiectasis.

Noisy breathing and rattly chests are common in younger children and do not necessarily indicate troublesome underlying pathology. They may upset parents or grandparents more than they do the child. Consider whether the symptoms affect the child’s day-to-day life and activities. Do they sleep normally, or are they woken by cough or wheeze? Do they manage regular attendance at school or nursery? Can they exercise normally, particularly PE and games? The infant equivalent of exercise is feeding, so ask if there is any difficulty with feeding, or slow weight gain.

Enquire particularly about the pattern and duration of any symptoms. Do they persist every day, or only occur episodically, e.g. with viral upper respiratory tract infections (URTIs)? A family or personal history of asthma or allergy such as eczema, hay fever or food allergy, may point towards asthma as the diagnosis. Ask about environmental precipitants such as passive smoking and exposure to dust or other inhaled allergens, including pollen and pet dander. Psychological and emotional factors need to be considered, as these are common triggers of airways obstruction.

Less common symptoms from respiratory disease include chest pain, vomiting and, in infants, apnoea. Young children with airways obstruction will sometimes refer to chest tightness as pain. Severe pain localized to the chest wall on deep breathing or coughing is called pleuritic pain, and is characteristic of acute lobar pneumonia with pleural involvement. Vomiting is frequent in young children with respiratory disease. Babies with gastro-oesophageal reflux may present with wheeze and cough; conversely, children with other respiratory conditions may vomit as a result of the large intrathoracic pressure swings affecting lower oesophageal (‘cardiac’) sphincter tone. Very young children, with conditions that usually cause cough, may present with apnoea instead. It is a common symptom in whooping cough and may be the presenting symptom in bronchiolitis, especially in ex preterm infants.

Remember that children with non-respiratory disease, such as diabetic ketoacidosis or panic attacks, may present with respiratory symptoms. On the other hand, some children with respiratory disease, especially pneumonia, may present with abdominal pain, or high fever alone, and little or nothing in the way of respiratory symptoms.

Examination

Use the scheme ‘inspection, percussion, palpation and auscultation’. Start your examination by observing the child at rest. Is there tachypnoea (see Table 10.1), recession or other evidence of respiratory distress, e.g. head bobbing in a baby or nostril flaring in a toddler? Does the child look anxious? Is there an audible noise during respiration (see Table 10.2)? Do not forget that tachypnoea may be due to fever or acidosis when there is no respiratory tract pathology.

Table 10.1 Respiratory rates at different ages

Age Breaths per minute
Neonate 40–60
Infant 30–40
5 years 20–25
10 years 15–20

Recession is a key physical sign in infants and young children. It describes the in-drawing of soft tissues around the chest by negative intrathoracic pressure generated by airway obstruction or reduced lung compliance. It may be seen in adults but is common in children because both soft tissues and the thoracic cage are more compliant. The resultant recession may be subcostal, intercostal or suprasternal. In addition, in neonates, the whole sternum may be sucked in – sternal recession, sometimes associated with grunting.

In older children you should complete a formal examination of the respiratory system including checking for clubbing (see Table 10.3) and cyanosis, percussion and auscultation. Look for chest deformity – Harrison’s sulci or pectus carinatum (‘pigeon chest’). These indicate chronically increased airway resistance – most commonly due to asthma.

Table 10.3 Causes of clubbing

System Cause
Cardiac Cyanotic congenital heart disease
Bacterial endocarditis
Respiratory Bronchiectasis
Cystic fibrosis/ciliary dyskinesia
Tuberculosis
Empyema/abscess, malignancy
Gastrointestinal Inflammatory bowel disease, chronic active hepatitis
Primary sclerosing cholangitis
Other Familial

In young children, particularly under 2 years, respiratory examination needs to be opportunistic and percussion is rarely of value. Audible crackles in the chest do not always mean lung consolidation or infection, particularly in the young child. They are often heard in wheezy children where they may be due to oedema and mucus in the small airways (see Table 10.4). Think about whether there are other signs of consolidation, such as reduced air entry or bronchial breathing. Examination of the ears and throat is a challenge in a fractious toddler – it is best left until last.

Table 10.4 Severity of respiratory distress

Grade Characteristics
Mild Tachypnoea
Mild recession
No effect on feeding or speech
Moderate Tachypnoea
Moderate or severe recession, struggles to feed,
cannot speak in full sentences
Oxygen may be needed to maintain saturation
Severe Tachycardia, gasping, speechless, frightened
May be pale and quiet or agitated and hypoxic despite oxygen
Chest may be silent and respiratory effort flagging
Impaired consciousness

Investigations

Upper respiratory tract infections

Upper respiratory tract infections (URTIs) may be summarized as snuffles, fever and misery.

Viral URTIs are the commonest conditions encountered in primary care. Adults are immune to most of the upper respiratory tract viruses in their immediate environment – they only produce symptoms when they contract a new virus. Children have to acquire immunity to a host of viruses in their first few years, and have, on average, six to ten episodes of infection annually. Changes of environment – such as starting at the nursery or school – will produce an even higher infection rate. Although often trivial illnesses in medical terms, the symptoms of snuffles, fever and sore throat may make young children thoroughly miserable.

Nasal obstruction may cause feeding problems in babies as they are obligate nose breathers. Symptomatic treatment includes paracetamol for the relief of discomfort and fever. Decongestant nose drops and oral decongestants are ineffective and best avoided. Saline nose drops are probably as effective as more expensive proprietary remedies.

Influenza

Flu, caused by the influenza virus types A, B and C, is a seasonal infection striking in the autumn and winter months. Influenza A is classified according to two key proteins – haemaglutinin (types H1–H3), important for infectivity, and neuraminidase (two types, N1 and N2), which determines viral replication. Neuraminidase is the target for the drugs oseltamivir and zanamivir. Influenza B also expresses neuraminidase, and hence is susceptible to antivirals. Influenza type C is a very mild, non-epidemic infection.

Type A is marked by antigenic drift, ensuring on-going susceptibility to seasonal flu, from year to year. Periodically, major antigenic shift occurs, probably due to recombination with avian and human flu types in pigs. Major antigenic changes herald worldwide pandemics, such as the recent H1N1 ‘swine flu’ pandemic. This predominantly affected young people (peak age 12–17 years) and was, for the most part, a mild disease, with symptoms indistinguishable from seasonal flu. However, in those with pre-existing conditions, the disease could be severe or fatal.

Influenza has a short incubation period (1–3 days), followed by sudden onset of fever, cough, coryza and myalgia. Vomiting, and less commonly diarrhoea, may occur. Myalgia is more common with influenza B, and creatine kinase may be elevated. Influenza is highly infectious, with rapid spread by respiratory droplet transmission. Symptoms typically remit in 5–7 days.

In those with severe disease, symptoms of rapidly progressive respiratory failure develop, typically 3–5 days after symptom onset, principally due to viral pneumonitis, but, in a third bacterial super-infection occurs. Multi-organ failure may supervene, and extracorporeal membrane oxygenation is required in severe cases.

Upper airways obstruction

Stridor and croup are important paediatric problems. The upper airway of children, being smaller than in adults, is more likely to obstruct with oedema of local tissues. Infections or allergies, which might produce hoarseness or loss of voice in an adult, may therefore produce alarming respiratory obstruction in a child. Acute severe stridor is an acute medical emergency. Management is described in Appendix I, p. 296.

Differential diagnosis of stridor

Croup, as is the diagnosis in Case 10.1, is the commonest cause of acute stridor. It occurs mainly in preschool children.

There is usually a viral prodrome, commonly with a barking cough. Parainfluenza virus is the commonest causative organism, and steroids are the mainstay of management. Meta-analysis of many trials has confirmed their efficacy and any child with croup severe enough to need hospital admission should receive steroids. Nebulized budesonide works more quickly than oral or parenteral steroids. In severe stridor, nebulized 1:1000 adrenaline (epinephrine), repeated as necessary, is useful as an emergency measure (see also Appendix I, p. 296).

Spasmodic croup describes the condition of a group of children with recurrent but often short-lived stridor. The condition is thought to be allergic – being commoner in those with other evidence of atopy.

Epiglottitis has become very rare following the introduction of Haemophilus influenzae b immunization. However, effectiveness of the vaccine has waned recently, prompting a booster, and children born abroad may not be immunized. Epiglottitis is a septicaemic illness, and good supportive care – as for any child with septicaemia – is needed. A third-generation cephalosporin such as ceftriaxone is used.

See Table 10.5 for the differences between croup and epiglottitis.

Table 10.5 The important differences between croup and epiglottitis

  Croup Epiglottitis
Organism Parainfluenza virus Haemophilus influenzae b
Age 6 months to 3 years 3–7 years
Prodrome URTI Usual Uncommmon
Onset Days Hours
Cough Present Often absent
Dysphagia Absent Severe with dribbling
Systemic Mildly unwell Toxic and ill
Posture No preference Sitting/leaning forward

Bacterial tracheitis is a rare cause of stridor. The child is usually extremely ill with co-existent septicaemia and pneumonia. Pus is seen in the trachea at intubation. Staphylococcus aureus is the most likely organism, but other organisms, such as Haemophilus, Moraxella or Streptococcus may be responsible.

Inhaled foreign bodies may present with stridor. Other presentations include the asymptomatic child following a choking episode, cough, wheeze or hoarseness. The history may not be definite but the diagnosis should always be considered in such children. Prompt recognition and removal is essential, as they may prove fatal. Delay in removal may also cause long-term morbidity, such as bronchiectasis. Ninety-five per cent of inhaled foreign bodies in children are organic, most commonly peanuts, and are not radio-opaque.

Anaphylaxis

Anaphylaxis can present with severe upper airways oedema leading to obstruction. Wheezing and collapse with hypotension may also occur. Severe cases may require intubation. Adrenaline (epinephrine), given either intramuscularly or intravenously, may be life-saving (see also Appendix I, p. 286). Steroids may be required for the wheeze but anti- histamines really only offer symptomatic relief for itching. Recent studies in young children have shown that milk and egg are the commonest causes, as opposed to nuts in older children and adults. Following an episode of anaphylaxis, thought should be given to allergy tests to help delineate the cause. Adrenaline (epinephrine) pens are also dispensed in increasing quantities for use in the community. Although seemingly a sensible precaution, they require thorough training, with a care plan in place for use in the school or nursery, and evidence suggests that they are rarely used.

Chronic upper airways obstruction

Congenital stridor is seen in infants, and is most commonly due to laryngomalacia. The cartilaginous parts of the larynx and trachea are less firm than usual, and partly obstruct the airway on inspiration. If severe it may cause failure to thrive due to feeding difficulties, and is often worse with viral URTIs.

Rarer causes include vascular rings compressing the trachea from outside, mediastinal masses such as neuroblastoma (see Chapter 7, p. 74) and intrinsic airway conditions such as haemangiomas and webs. Babies with anything other than very mild stridor should have a plain chest X-ray and a barium swallow. A barium swallow is more effective than echocardiography in picking up vascular rings. Moderate to severe stridor requires direct laryngoscopy to look for intrinsic lesions such as airway haemangiomas. The prognosis for laryngomalacia is excellent, with the noisy breathing diminishing with age as the cartilage strengthens.

Snoring and obstructive sleep apnoea

Snoring is relatively common in children, and is usually benign. Snoring is characteristically episodic, and associated with upper respiratory tract infection, rhinitis or nasal obstruction. The commonest cause of chronic snoring is adenotonsillar hypertrophy. Snoring that is persistent and loud may be indicative of airway obstruction, which, in turn, may predispose to obstructive sleep apnoea (OSA).

OSA is relatively uncommon in children (incidence 0.8–2.0%). The commonest cause is marked adenotonsillar hypertrophy, typically presenting between 3 and 6 years of age. Congenital disorders that narrow the airway, such as achondroplasia, and disorders with reduced muscle tone, such as Down syndrome, predispose to OSA. In older children, morbid obesity is the commonest cause.

OSA may produce a range of symptoms. In the younger child, failure to thrive and behavioural problems may result. In severe cases, particularly in association with obesity, pulmonary hypertension and cor pulmonale may result from chronic hypoxia.

In addition to snoring, parents may report gasping, or pauses in breathing during sleep. Behavioural problems such as headaches, ADHD and enuresis are more common in children with OSA. Day-time sleepiness is less common than in adults.

Clinical signs may include visible tonsillar enlargement, glue ear (secondary to adenoidal hypertrophy), nasal obstruction with mouth breathing, and nasal speech and obesity.

Any child with chronic snoring should be evaluated with overnight pulse oximetry. Recurrent desaturations below 92% are suggestive of OSA. In the first instance, adenotonsillectomy is recommended. If symptoms of OSA persist, a formal sleep study in a specialist centre is usually recommended to confirm the diagnosis. Overnight continuous positive airway pressure (CPAP) may be appropriate for refractory cases.

Chronic cough

Chronic cough is defined as being present for more than 3 weeks. It has many causes. It may be associated with infection or inflammation, or it may be habitual, in which case the cough has a characteristic ‘honking’ or ‘brassy’ quality.

The assessment should inquire about the nature of the cough, any sputum production, and any associated symptoms or relevant past medical history. A paroxysmal cough suggests pertussis; night-time, or exercise-induced cough might suggest asthma; sputum production and fever suggest bronchiectasis or tuberculosis. Relationship to posture or feeds may occur with gastro-oesophageal reflux. A history of choking may indicate an inhaled foreign body. Immune deficiency or cystic fibrosis will usually cause failure to thrive. Tracheo-oesophageal fistula (see Chapter 17, p. 259), is associated with a characteristic ‘TOF cough’.

Pertussis

Pertussis, or whooping cough, is caused by Bordatella pertussis. It invades the pulmonary ciliary epithelium causing bronchial congestion and inflammation, with peribronchial lymphoid hyperplasia (catarrhal stage 1–2 weeks). Wide-spread epithelial necrosis then ensues, with the characteristic coughing bouts (paroxysmal stage 2–4 weeks), and predisposes to atelectasis and bronchopneumonia. Paroxysms of coughing with a terminal ‘whoop’ are characteristic (as in Case 10.2). Children are unable to catch their breath and may become cyanosed. Apnoea occurs in young infants. Vomiting is common. Pneumonia accounts for 80–90% of deaths from pertussis. Seizures (3%) and encephalopathy (1%) may occur. The convalescent phase lasts from 1–2 weeks to many months. Use of antibiotics in the catarrhal stage may shorten the illness but, if started in the convalescent stage, has no effect on the duration of illness, although infectivity to others is alleviated. In adults and older children, who are the usual sources of infection, the cough is a dry, repetitive, ‘staccato’ cough.

Large-scale outbreaks of whooping cough in Britain and the USA in 2011-12, to levels not seen for over 50 years, have led to concerns that the current whooping cough immunization schedule (see Chapter 1, p. 3) does not provide long-lasting immunity. The introduction of a further booster immunization for secondary school children and pregnant women is under consideration. Booster immunizations for healthcare workers have now been recommended.

The wheezy child

Wheezing is an extremely common symptom, occurring in about half of all children at some time in childhood. Many of these children have isolated episodes of wheezing in association with viral infections. Twenty to thirty per cent of children have either persistent or recurrent wheezing and only half of these turn out to have true ‘asthma’. Attempts to delineate diagnostic groups more clearly are hampered by the lack of a truly robust definition of asthma in childhood. There is a group of children who wheeze only with viruses and who respond to bronchodilators, but lack interval symptoms and fail to respond to inhaled steroids. Definitions of asthma relying purely on bronchial hyper-reactivity will include those children with viral wheezing and overestimate asthma prevalence. Questionnaire studies of asthma prevalence are hampered by the same difficulties.

In practice this means that any child with acute wheezing can be treated in a similar fashion, but chronic management will depend more on the likely cause of the wheezing.

Bronchiolitis

Bronchiolitis is a term used to describe an acute respiratory infection, in children under 1 year, where wheezing may be present (as in Case 10.3). The cardinal signs are crepitations and expiratory wheeze with recession and, if severe, cyanosis. The baby initially has snuffles, which progress to a characteristic dry, hacking cough. RSV is the commonest cause of bronchiolitis, but is not a prerequisite for diagnosis. Treatment is supportive therapy with oxygen, nasogastric feeding and occasionally CPAP or even ventilation in those most severely affected (1–2%). Bronchodilators may help those with prominent wheeze, but controlled trials have failed to show clinical benefit of these or other treatments such as steroids, antibiotics, adrenaline (epinephrine) or specific antiviral treatment. Prophylactic treatment with the monoclonal antibody palivizumab is advocated for some high-risk infants, particularly those on home oxygen, to prevent life-threatening bronchiolitis.

In some parts of the world, the term bronchiolitis is used to describe any wheezy young child, which makes interpretation of the literature difficult. However, 50% of infants with bronchiolitis wheeze with subsequent viruses, as in the episodic wheezing group below. A proportion of these have atopy and would develop asthma anyway, so diagnostic categories are further blurred!

Persistent wheezing

Symptoms of chronic wheezing follow two common patterns, but with some crossover: episodic wheeze and chronic wheeze.

Chronic wheeze

This is classical asthma with frequent, often daily, symptoms, affecting sleep and exercise (as in Case 10.4). Background atopy is common. Management is as outlined in current British guidelines for asthma management, with inhaled steroids being the mainstay. If there is doubt over a diagnosis of asthma, particularly in children too young to provide peak flows, a trial of inhaled steroids is a sensible way forward. Review the situation after 6 to 8 weeks – do not continue inhaled steroids if they are not helping.

See Figures 10.2 and 10.3 for a summary of stepwise management in children.

image

Figure 10.2 Summary of stepwise management in children aged less than 5 years.

(Reproduced from British Guideline for the Management of Asthma.)

image

Figure 10.3 Summary of stepwise management in children aged 5–12 years.

(Reproduced from British Guideline on the Management of Asthma.)

Lower respiratory tract infections

The hallmarks of lower respiratory tract infection (LRTI) are fever, breathlessness and cough. Acute LRTIs in childhood are mostly caused by viruses. Pneumonia tends to be a term used loosely when consolidation is present on a chest X-ray. Even in children with clear-cut consolidation present, a virus is still a common cause. However, as bacterial LRTI may have severe consequences, and it is difficult clinically and radiologically to tell the difference, antibiotics are routinely used for any LRTI.

LRTI in childhood tends to present in two ways. ‘Atypical pneumonia’ has been a term used for a pattern of symptoms with fever, cough and variable with fever, cough and variable breathlessness, with or without evidence of airways obstruction in the form of recession. Crackles are audible but not usually bronchial breathing. The X-ray looks patchy, with reticular/nodular shadowing. Viruses are a common cause but bacterial LRTI with mycoplasma or pneumococcus may present this way. In primary care, amoxicillin is usually the recommended first-line antibiotic. In secondary care, if the child is unwell, treatment to cover mycoplasma is appropriate; azithromycin or clarithromycin are commonly used. This presentation is more common than classical lobar pneumonia, so the term ‘atypical’ tends to be avoided now.

Classical lobar pneumonia is due to extensive alveolar consolidation, and airways obstruction is not seen. The child presents unwell with a fever and there may be no symptoms to point to the respiratory tract (as in Case 10.5).

A chest X-ray should always be included in a septic screen of a child with no clue as to the aetiology of the infection. Pleuritic chest pain is common, and respiratory distress with nasal flaring, and sometimes cyanosis, is a late symptom. The classical signs of a dull percussion note, reduced air entry, bronchial breathing and crackles may be heard, especially if it is lower lobe in origin. In upper-lobe pneumonias, in particular, no signs may be found and diagnosis is based on the radiology. If the child is toxic with a high fever, or has a pleural effusion, admission for intravenous therapy is needed. In the UK, benzylpenicillin is the first-line treatment, but in some parts of the world pneumococcal resistance is a problem and other agents are required.

Most children respond to treatment in 24–48 hours and can be allowed home on oral antibiotics. Beware of children whose fever does not settle in 48 hours, particularly if they have a pleural effusion. Empyema is still a relatively common complication. Controversy exists as to the best management, with some advocating early surgical intervention and others the insertion of a fine chest drain and the use of urokinase. Either way, the long-term outlook is usually good.

Uncommon serious infections

Cystic fibrosis

Cystic fibrosis (CF) is the commonest genetic condition seen in Caucasian populations. It is inherited in an autosomal recessive fashion with the CF mutation present on the long arm of chromosome 7. Over a thousand mutations are known, with AF508 being the commonest, accounting for 80% of mutations in the UK. Affected individuals may have compound heterozygosity for two different mutations. The cellular transport mechanism that is affected is primarily a chloride channel – cystic fibrosis transmembrane regulator (CFTR). CFTR maintains an ionic gradient over the surface of the cells lining the epithelium, which keeps the cell surface moist. When CFTR malfunctions, respiratory and other epithelial surfaces dry out, resulting in tenacious, viscid secretions (see Box 10.1).

Newborn screening for CF was introduced across the UK from 2007 but should be remembered as a possibility in children born before that date. Neonatal screening is based on newborn blood spots, which are screened first for raised immunoreactive trypsin (high concentrations of trypsin develop in obstructed pancreatic ducts, leading to pancreatic inflammation, and elevation of serum trypsin; the elevation persists for several weeks after birth), and then specific common genetic mutations. Screening is not 100% effective though, and one should remain aware of the possible clinical presentations.