Rib cage and chest shape

The cross-sectional shape of the infant thorax is cylindrical and not elliptical as in adolescents or adults. The ribs of the newborn infant are relatively soft and cartilaginous compared with the more rigid chest wall of older children and adults. They are also placed horizontally in relation to the sternum and vertebral column compared with the more oblique rib angle of adults (Fig. 10.1). The bucket handle rib movement seen in older children and adults is therefore not possible. As the infant grows, and begins to develop an upright posture, the ribs develop a more oblique angle and the transverse diameter of the rib cage increases. The adult chest shape is achieved by 3 years of age (Openshaw et al 1984).

Figure 10.1 Normal chest radiograph.

The intercostal muscles are poorly developed in infancy and contraction of the intercostal muscles is inefficient at improving thoracic volumes either by increasing the anteroposterior or transverse diameters of the chest. Increased ventilatory requirements have to be met by increasing the respiratory rate rather than depth (Konno & Mead 1967).

Diaphragm

The angle of insertion of the infant diaphragm is horizontal compared with older children or adults, placing it at a mechanical disadvantage. The infant diaphragm has a lower relative muscle mass and a lower content of high-endurance muscle fibres, and thus is much more vulnerable to fatigue.

Maximal diaphragmatic activity during severe respiratory distress or respiratory obstruction leads to an inward movement of the lower rib cage instead of a downward movement of the diaphragm, as well as intercostal and sternal recession (Muller & Bryan 1979). Despite these disadvantages, the diaphragm is the main muscle of inspiration in the infant, since the intercostals are poorly developed. Ventilation in the infant is also more affected by impaired diaphragmatic function, for example by abdominal distension, hepatomegaly or phrenic nerve damage.

Preferential nasal breathing

The shape and orientation of head and neck in babies (large head, prominent occiput, short neck, large tongue, smaller retracted lower jaw, high larynx) mean that the airway is prone to obstruction in young infants. Young infants up to about 6 months of age are preferential nasal breathers and studies suggest that up to half of all neonates are unable to breathe through their mouths, except when crying, for the first few weeks of life (King & Booker 2004) The small nasal passages account for between 30% and 50% of the total airway resistance in neonates. The narrowest portion of the nasal airway has a cross-sectional area of about 20 mm². Therefore, even a small amount of swelling or obstruction of the nasal passages of infants compromises breathing considerably and causes a disproportionate and detrimental effect on the work of breathing. Some young infants with upper respiratory tract infections and partial obstruction of their nasal passages can develop respiratory distress.

Position of larynx

In the newborn infant, the larynx and hyoid cartilage are higher in the neck and closer to the base of the epiglottis, being at the level of C3 in a premature infant and C4 in a child compared with C5–6 in the adult. The larynx descends with age, but its high position enables the infant to feed and breathe simultaneously for approximately the first 4 months of age.

This high position also provides some protection of the airway in infants younger than 4–6 months because it acts as a valve, which helps keep food in the mouth until the pharyngeal swallow is initiated. The airway has less anatomical protection as the larynx assumes its lower position in the neck and is not as directly protected by the epiglottis. Then, poor closure of the airway or partial paralysis of the vocal folds may become more evident and coughing, choking or aspiration may occur.

Airway diameter

The neonatal trachea is short (4–9 cm) and directed downward and posteriorly. The diameter of the trachea in the newborn is 4–5 mm and the diameter of an infant trachea is only about one-third that of an adult. This makes respiratory resistance higher and the work of breathing greater. Since the resistance to airflow through a tube is directly related to the tube length and inversely related to the fourth power of the radius of the tube, halving the radius of the trachea will increase its resistance (reduce flow) 16 times. Tracheal swelling as a result of endotracheal intubation or suction can therefore dramatically increase resistance to breathing. These factors give the lungs less reserve, so that a well-oxygenated infant with upper airway obstruction can become cyanotic in a matter of seconds.

In contrast to adolescents and adults, the narrowest part of the infant’s airway is not the vocal cords, but the cricoid ring. Thus an uncuffed endotracheal tube provides a larger internal diameter compared with a cuffed tube and in children will successfully seal against in the circular subglottic ring. However, the inflexible cricoid ring also leaves children more vulnerable to mucosal oedema and post-extubation stridor. The right main bronchus is less angled than the left, making right mainstem intubation more likely.

At birth there is no further increase in the number of airways formed but there is growth and development in their size. In the first few years of life there is a significant increase in the diameter of the larger, more proximal airways (Hislop & Reid 1974). The smaller, more distal airways do not increase in diameter until nearer 5 years of age. This higher peripheral airways resistance is exacerbated by respiratory infections, which cause inflammation of the airways, for example in bronchiolitis, or in the presence of secretions.

Bronchial walls

The bronchial walls are supported by cartilage, which begins to develop from 12 weeks’ gestation and continues throughout childhood. The cartilaginous support of an infant’s airways is much less than that of an adult, and predisposes the airways to collapse. The bronchial walls contain proportionally more cartilage, connective tissue and mucous glands than do those of adults, but less smooth muscle; this makes the lung tissue less compliant. The lack of bronchial smooth muscle, particularly in the smaller bronchioles, may be one reason for the lack of response to bronchodilators under the age of 12 months. The β-receptors in infants are also immature, which further reduces any response to β-adrenergic bronchodilator therapy (Reid 1984). The high proportion of mucous glands in the major bronchi of infants makes the airways more susceptible to mucus obstruction.

Cilia

At birth the cilia are poorly developed, which increases the risk of secretion retention, especially in the premature infant. The airway obstruction caused by secretions in a neonate is much greater than in an adult whose airways are relatively large.

Alveoli and surfactant

The respiratory system is not fully developed at birth, even in the term neonate, and postnatal maturation continues for a significant time. Although by 20–27 weeks’ gestation lung acinar have formed, several types of epithelial cells can be differentiated, and the air–blood barrier is thin enough to support gas exchange; true alveoli develop only after about 36 weeks’ gestation. A term newborn has an average of 150 million alveoli. The remainder of the eventual average of 400 million alveoli develop after birth, the vast majority within the first 2 years of life. Both the number and size of alveoli continue to increase postnatally until the chest wall stops growing. By 4 years of age, the adult number of 300 million may exist, although growth can continue until 7 years of age. The smaller alveolar size of an infant makes the infant more susceptible to alveolar collapse, and the smaller number of alveoli reduces the area available for gaseous exchange (Reid 1984).

Pulmonary surfactant is a mixture of phospholipids (90%) and apoproteins (10%), which act to reduce surface tension at the air–liquid interface in the alveolus, thereby preventing collapse of lung parenchyma at the end of expiration. Type II alveolar cells synthesize and secrete surfactant from 23 to 24 weeks’ gestation. In preterm newborns, a deficiency of surfactant is a major factor in the development of neonatal respiratory distress syndrome (RDS). Male gender is a risk factor for neonatal RDS, bronchopulmonary dysplasia (BPD) and mortality. Boys with neonatal RDS seem to have more health problems than girls during the neonatal period.

Collateral ventilation

Collateral ventilation is the means by which a distal lung unit can be ventilated, despite blockage of its main airway. Collateral ventilatory pathways are achieved by a network of interconnecting pathways linking different structures. Respiratory bronchioles are linked by channels of Martin. Canals of Lambert connect respiratory and terminal bronchioles with alveoli and their ducts; and adjacent alveoli are joined by openings in the alveolar wall, called pores of Kohn (Menkes & Traystman 1977). However, none of these pathways exists at birth. The pores of Kohn develop between years 1 and 2, and the canals of Lambert do not appear until about 6 years of age. The collateral ventilatory channels between alveoli, respiratory bronchioles and terminal bronchioles are poorly developed until 2 and 3 years of age, predisposing towards alveolar collapse.

Internal organs and lymphatic tissue

The lymphatic tissue (adenoids and tonsils) may be enlarged in the infant and the tongue is also relatively large. These factors may contribute to upper airway obstruction. The heart and other organs are also relatively large in infants, leaving less space for lung expansion. The heart can occupy up to half the transverse diameter of the chest in chest radiographs.

Height and exposure to air pollution

Because children breathe more rapidly compared with adults and because they spend more time outdoors being physically active, they tend to be more exposed to outdoor air pollution and allergens than do adults and have greater deposition of particulate matter. Their reduced height means they are also more exposed to vehicle exhausts and heavier pollutants that concentrate at lower levels in the air. There is substantial evidence linking air pollution with respiratory health problems and children are more vulnerable (Brauer et al 2007, Pénard-Morand et al 2005).

Respiratory compliance

Respiratory compliance is a measure of the pressure required to increase the volume of air in the lungs and reflects a combination of lung and chest wall compliance. The lung compliance of a child is comparable to that of an adult, being directly proportional to the child’s size. However, compliance is reduced in the infant because of the high proportion of cartilage in the airways. The premature infant, who lacks surfactant, demonstrates a further significant decrease in compliance. The chest wall of an infant is cartilaginous and therefore very soft and compliant in comparison with the more calcified and rigid adult structure. The intercostal muscles are also less well equipped to stabilize the rib cage during diaphragmatic contraction. Neonates therefore have an imbalance between a relatively low outward recoil of their chest wall and normal inward elastic recoil, which means that they are prone to airway collapse. An awake, spontaneously breathing neonate will maintain its functional residual capacity (FRC) by active measures including laryngeal braking, the initiation of inspiration before the end of passive expiration (intrinsic PEEP) and persistent inspiratory muscle activity throughout the respiratory cycle. These active mechanisms are lost during anaesthesia and result in a fall in FRC, airway closure, atelectasis and ventilation/perfusion mismatch.

Closing volume

The closing volume is the lung volume at which closure of the small airways occurs. This volume plus the residual volume (the volume of gas left in the lungs following maximum expiration) is known as the closing capacity (CC). In the adult, CC is less than FRC, i.e. the volume of gas left in the lungs following tidal expiration, whereas in the infant it is greater than FRC. The higher closing volumes apparent in infants are due to greater chest wall compliance and reduced elastic recoil of the lungs than in the adult. Therefore, airway closure may occur before the end of expiration, e.g. during expiratory chest vibrations, putting the infant at a much greater risk of developing widespread atelectasis, especially in the presence of lung disease, where lung volume is further reduced. In the event of respiratory distress, the infant grunts on expiration, adducting the vocal cords in an attempt to reduce the amount of gas expired, thus maintaining a higher FRC and minimizing alveolar collapse (Pang & Mellins 1975). Re-inflation of alveoli, once collapsed, is more difficult in the infant, who has to work considerably harder to overcome the effects of the compliant chest wall.

Ventilation and perfusion

In the adult, both ventilation and perfusion are preferentially distributed to the dependent lung. The best gas exchange and ventilation/perfusion match will therefore be in the dependent region of the lung (Zack et al 1974). In the infant, however, ventilation is preferentially distributed to the uppermost lung (Davies et al 1985), whereas the perfusion remains best in the dependent regions. This leads to greater gas exchange in the uppermost lung (Heaf et al 1983) but an imbalance between ventilation and perfusion (Bhuyan et al 1989). In acutely ill children with unilateral lung disease, oxygenation may be optimized by placing the ‘good’ lung uppermost. However, this is contrary to the goal of improving ventilation to the diseased lung and facilitating secretion clearance, in which positioning and postural drainage would require the diseased lung to be uppermost. The therapist would have to balance their decision based on the stability, tolerance and current therapeutic priorities.

The difference in ventilation distribution between infants and adults is most likely due to the more compliant rib cage of the infant, which compresses the dependent areas of lung. In addition, while in the adult the weight of the abdominal contents provides a preferential load on the dependent diaphragm and therefore improves its contractility, in the infant this does not happen. The effect on both hemidiaphragms is similar, due to the abdomen being so much smaller and narrower (Davies et al 1985). It has been shown in adults that, when the diaphragm is inactivated, e.g. when ventilated under anaesthetic, the ventilation distribution changes to that of an infant (Rehder et al 1972). It is not yet known exactly when the ventilation distribution in the infant changes to that of an adult, but it may be as late as 10 years of age.

Oxygen consumption, cardiac output and response to hypoxia

Infants have a higher resting metabolic rate than adults and consequently have a higher oxygen requirement. Children have a higher cardiac output and oxygen consumption per kilogram than adults; in infants this may exceed 6 ml/kg/min, twice that of adults. They support this higher output with a higher baseline heart rate but lower blood pressure than adults.

Neonatal myocardium has a large supply of mitochondria, nuclei and endoplasmic reticulum to support cell growth and protein synthesis, but these are non-contractile tissues, which render the myocardium stiff and non-compliant. This may impair filling of the left ventricle and limit the ability to increase the cardiac output by increasing stroke volume (Frank Starling mechanism). Stroke volume in infants is therefore relatively fixed and the only way of increasing cardiac output is by increasing heart rate.

The sympathetic nervous system is not well developed predisposing the neonatal heart to bradycardia. An infant responds to hypoxia with bradycardia and pulmonary vasoconstriction, whereas the adult becomes tachycardic with systemic vasodilation. The bradycardic response in infants is probably due to myocardial hypoxia and acidosis, but leads to an immediate reduction in cardiac output and the development of further hypoxia.

Although anatomical closure of the foramen ovale can occur as early as 3 months of age, the channel remains ‘probe patent’ in 50% of children up to 5 years of age, and persists in about 30% of adults. Similarly, anatomical closure of the ductus arteriosus usually occurs between 4 and 8 weeks of age. Any stimulus, such as hypoxia or acidosis, that causes an increase in pulmonary vascular resistance during the neonatal period may allow these two potential channels to reopen, resulting in right-to-left shunting and increasing hypoxia (King & Booker 2004).

Muscle fatigue

The respiratory muscles of infants tire more quickly than those of adults due to a much smaller proportion of fatigue-resistant muscle fibre (Keens & Ianuzzo 1979). There are two main muscle fibre types, type I and type II. Type I muscle fibres are slow twitch, high oxidative and slow to fatigue. Type II fibres are fast twitch, slow oxidative and tire quickly. Of the muscle fibres in the adult diaphragm, 55% are type I compared with only 30% in the infant. Premature infants tire even more easily as, at 24 weeks’ gestation, only 10% of their muscle fibres are fatigue resistant (Muller & Bryan 1979). Excessive muscle fatigue results in apnoea. By 12 months of age the number of type I fibres equals that of an adult.

Breathing pattern and rapid eye movement sleep

Irregular breathing patterns and episodes of apnoea are relatively common in neonates, especially if premature, and are related to immature cardiorespiratory control. Short spells of apnoea can be considered normal in these circumstances, but need careful monitoring as they may reflect hypoxic conditions.

During rapid eye movement (REM) sleep there is a reduction in postural tone and tonic inhibition of the infant’s intercostal muscles such that the rib cage is even less well equipped to counteract the contraction of the diaphragm during inspiration (Muller & Bryan 1979). This reduces the efficiency of respiration, causes a drop in functional residual capacity and increases the work of breathing, predisposing the infant to apnoeic episodes (Muller & Bryan 1979). The premature infant is most at risk, spending up to 20 hours a day asleep, 80% of which may be in active REM sleep compared with 20% in adult sleep.

Response to cold

Paediatric patients have an increased surface area per kilogram and lose heat to the environment more readily than adults. This is compounded by cold intravenous fluids, dry anaesthetic gases and exposure. Non-shivering thermogenesis in brown adipose tissue is the major mechanism of heat production during the first few months of life. Brown fat is specialized tissue located in the posterior of the neck, along the interscapular and vertebral areas, and surrounding the kidneys and adrenal glands. Metabolic heat production can increase up to two and a half times during cold stress. Shivering is a less economical form of heat production but does occur in severely hypothermic neonates. Hypothermia is a serious problem that can result in increased oxygen consumption, cardiac irritability and respiratory depression (King & Booker 2004).

Clinical signs

Clinical signs of respiratory distress are listed in Box 10.1.

Box 10.1 Clinical signs of respiratory distress

Recession

Recession

– intercostal

– subcostal

– sternal

Nasal flaring

Tachypnoea

Expiratory grunting

Stridor

Cyanosis

Abnormal breath sounds

Cardiac

Tachycardia/bradycardia

Hypertension/hypotension

Other/general

Neck extension

Head bobbing

Pallor

Reluctance to feed

Irritability/restlessness

Altered conscious level

Headache

Recession occurs when high negative intrathoracic pressure during inspiration pulls the soft, compliant chest wall inward. It may be sternal, subcostal or intercostal. Mild recession may be normal in preterm infants but in older infants is a sign of increased respiratory effort.

Nasal flaring is a dilatation of the nostrils by the dilatores naris muscles and is a sign of respiratory distress in the infant. It may be a primitive response attempting to decrease airway resistance.

Tachypnoea (respiratory rate greater than 60 breaths/min) may indicate respiratory distress in infants. Normal values are listed in Table 10.1.

Table 10.1 Normal values

Grunting occurs when an infant expires against a partially closed glottis. This is an automatic response which increases functional residual capacity in an attempt to improve ventilation.

Stridor is heard in the presence of a narrowing of the upper trachea and/or larynx. This may be due to collapse of the floppy tracheal wall, inflammation or an inhaled foreign body. It is most commonly heard during inspiration, but in cases of severe narrowing it may be heard during both inspiration and expiration.

Cyanosis refers to the bluish colour of the skin and mucous membranes caused by hypoxaemia. In infants and young children it is an unreliable sign of respiratory distress as it depends on the relative amount and type of haemoglobin in the blood and the adequacy of the peripheral circulation. For the first 3–4 weeks of life, the newborn infant has an increased amount of fetal haemoglobin, which has a higher affinity for oxygen than adult haemoglobin. The result is a shift of the oxygen saturation curve to the left in infants.

Auscultation of the infant and young child is sometimes complicated by the easy transmission of sounds. In the infant who is ventilated, referred sounds such as water in the ventilator tubing may be transmitted to the chest. In the older child, secretions in the nose or throat may lead to referred sounds in both lung fields. Wheezing in the younger child or infant may be due to bronchospasm, but could also be due to retained secretions partially occluding smaller airways. It is sometimes very difficult to hear breath sounds in the spontaneously breathing preterm infant.

Cardiac manifestations of respiratory distress include an initial tachycardia and possible increase in systemic blood pressure. This changes with worsening hypoxia to bradycardia and hypotension.

Neck extension in an infant with respiratory distress may represent an attempt to reduce airway resistance.

Head bobbing occurs when infants attempt to use the sternocleidomastoid and the scalene muscles as accessory muscles of respiration. It is seen because the relatively weak neck extensors of infants are unable to stabilize the head.

Pallor is commonly seen in infants with respiratory distress and may be a sign of hypoxaemia or other problems, including anaemia.

Reluctance to feed is often associated with respiratory distress and infants may need to take frequent pauses from sucking when tachypnoeic.

Alterations in levels of consciousness should be noted. A reduction in activity may be due to neurological deficit or as a result of opiate analgesia but may also be due to hypoxia. It may be accompanied by an inability to feed or cry. Irritability and restlessness may also be indicative of a hypoxic state.

Other relevant observations

The behaviour of a child can often give important clues about their respiratory status. Agitation or irritability may be a sign of hypoxia, while the child in severe respiratory distress may be withdrawn and lie completely still.

It is important to note muscle tone in the infant or child with respiratory distress. A hypotonic child may have increased difficulty with breathing, coughing and expectorating, while hypertonia may also be associated with difficulty in clearing secretions.

Abdominal distension can cause or exacerbate respiratory distress, because the diaphragm is placed at a mechanical disadvantage. In infants this is of greater concern as the diaghragm is the primary muscle of respiration.

Precautions for chest percussion and vibratory techniques

In children with dietary deficiencies, liver disease, bone mineral deficiency (e.g. rickets) or coagulopathies, manual techniques should be applied with caution. Manual techniques may not be appropriate in extremely premature infants and specific issues related to this group of patients are discussed later.

Chest percussion has been reported to cause an increase in bronchospasm in adults with chronic lung disease (Campbell et al 1975, Wollmer et al 1985). Premedication with bronchodilator therapy may reduce this effect but in severe cases percussion should be avoided.

Airway clearance for children with neurological and neuromuscular impairment

Impaired cough, as a consequence of weakness from neuromuscular disease such as Duchenne muscular dystrophy and spinal muscular atrophy or neurological impairment, can cause serious respiratory complications including atelectasis, pneumonia, airway obstruction and acidosis (Miske et al 2004). Chronic respiratory insufficiency and respiratory failure will ultimately result from chronic weakness of respiratory muscles, shallow breathing and ineffective cough. For these children, independently performed airway clearance techniques are not usually feasible, but options such as the ‘cough assist’ (mechanical insufflation/exsufflation device) and other non-invasive forms of positive pressure ventilation are safe and well tolerated in this client group, with growing evidence to support their efficacy (Chatwin et al 2003, Panitch 2006, Vianello et al 2005). They are discussed more comprehensively in Chapters 5 &11. Not all patients with neuromuscular disease are good candidates for the use of non-invasive respiratory aids. Potential contraindications include an inability to manage oropharyngeal secretions, mental status changes or cognitive impairment, and cardiovascular instability. For some patients, including those with the most severe spinal muscular atrophy, sole reliance on non-invasive methods of assisted cough and ventilation is inadequate, and they may require repeated episodes of intubation and mechanical ventilation in the intensive care unit to prolong survival (Birnkrant 2002).

Saline instillation

Saline instillation into the tracheal tube of ventilated patients aims to loosen thick or sticky secretions to facilitate easy removal with suction (Schreuder & Jones 2004). Evidence for the practice is variable and therefore saline should be used only where there is a clear indication. Some suggest that saline instillation at best is not effective and at worst is harmful (Blackwood 1999, Hagler & Traver 1994, Kinloch 1999, McKelvie 1998, Ridling et al 2003), while others suggest it is well tolerated even in infants and may be helpful in removing secretions adherent to the chest wall (Shorten et al 1991). Other mucolytics (N-acetylcysteine) in aliquots of 0.5–5 ml may be used to enhance secretion clearance. Larger quantities of irrigants are sometimes used as part of bronchoalveolar lavage procedures.

Aetiology

Children are more likely to develop asthma if parents or close relatives are asthmatic or atopic. There is an important link between atopy and bronchial hyperreactivity, and children with asthma often have other atopic features such as eczema, food allergy, hay fever or urticaria. Exposure to specific allergens such as house dust mite, pollen and animal dander can precipitate bronchospasm and wheeze. Exercise, particularly running, can precipitate an acute attack (exercise-induced asthma, EIA), as can emotional upset or upper respiratory tract infections.

Management

The mainstay of asthma treatment is drug therapy. There are agreed guidelines on the management of asthma (British Thoracic Society & Scottish Intercollegiate Guidelines Network (SIGN) 2003, National Asthma Education and Prevention Programme (NAEPP) 2002). The aims of therapy are to obtain optimal asthma control with few or no symptoms, undisturbed sleep, normal lung function with no limitation to daily activity and no severe, acute exacerbations. Poor asthma control has been attributed to suboptimal adherence to treatment guidelines both by physicians and families (Rabe et al 2004).

Short-acting inhaled β₂-agonists may be all that is required in children who have mild intermittent asthma, but inhaled corticosteroids are the mainstay of asthma therapy in those with persistent symptoms and are given in addition to short-acting β₂-agonists. Administration of corticosteroids by the inhaled route is safer and results in fewer systemic effects. It is important when using inhaled corticosteroids in children that growth is carefully monitored. In more severe asthma, long-acting β₂-agonists should be added to the treatment regimen. Leukotriene receptor antagonists may also be useful in a proportion of cases. Higher doses of inhaled corticosteroids may be needed. The use of continuous (preferably alternate day) oral steroids for prophylaxis is rarely needed nowadays. More severely affected children may require them intermittently on a continuous daily basis, for short periods, during acute exacerbations.

Inhalation of asthma medications provides effective topical therapy, which usually requires smaller doses and has fewer systemic effects. However, the method of drug delivery is very important and has been extensively reviewed (O′Callaghan 2000).

The choice of device depends both on the drug to be delivered and the patient, particularly in relation to age. In children the preferred method for delivery of both inhaled corticosteroids and β₂-agonists is by metered dose inhaler (MDI) along with a spacer device. Metered dose inhalers can be manually or breath-actuated and contain a mixture of propellant and drug which is emitted at a high velocity. Breath-actuated devices require an adequate inspiratory flow to trigger the device and the manual devices require coordination of the actuation of the device with inspiration. This makes them inherently difficult to use in children and therefore a valved spacer device should be incorporated into the system. The spacer allows the infant or child to inhale from a reservoir of drug within a chamber.

In babies, a facemask is required and should be held gently over the nose and mouth with the device held upright, at an angle greater than 45°, to ensure the valve is open. The drug can then pass effectively through the open valve to be inhaled (Fig. 10.7A & B). Once the child is older (usually from the age of 2 or 3), the spacer device can be used conventionally with a mouthpiece (Fig. 10.7C). The click of the valve opening will be heard with each breath. It should be noted that different spacer devices have been shown to deliver varying drug doses (Barry & O′Callaghan 1996).

Figure 10.7 Administration of bronchodilator by spacer device to (A) an infant; (B) a teddy bear, to familiarize a young child with the device; (C) a young child.

Nebulized drug delivery systems for asthma are now rarely used in the home setting. They may be used in circumstances where medication cannot be delivered effectively using an MDI and spacer and in severe cases or during an acute exacerbation. It is preferable to use a mouthpiece (if the child is able) so as to avoid drug deposition on the face.

Children with a severe asthma attack usually display signs of acute respiratory distress; they may not be able to complete a sentence in one breath or may not be able to talk, and infants show difficulty in feeding due to breathlessness. The respiratory rate is usually high (>30/minute age 5 years and above, >50/minute – age 2–5 years) and the child is tachycardic. Obvious wheezing may not necessarily be present. In life-threatening attacks, when airway obstruction in the presence of hyperinflation is severe, the airflow may be so low that wheezing is not heard, the respiratory rate is lower than expected and the chest is ‘silent’. The child may be cyanotic and is often exhausted. Children with either severe or life-threatening asthma require immediate admission to hospital. It is important to note that if nebulized bronchodilator therapy is given during an acute attack it should be oxygen driven to avoid hypoxaemia (Inwald et al 2001).

Exercise-induced asthma

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