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Examining the respiratory system 

Examining the respiratory system
Chapter:
Examining the respiratory system
Author(s):

Jeremy Hull

, Julian Forton

, and Anne Thomson

DOI:
10.1093/med/9780199687060.003.0001
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Introduction

Examining the chest is part of the routine physical examination of all children who are unwell. Most doctors are expert at identifying the abnormal signs that indicate disease. This short section provides the background to a common language so that clear descriptions can be given to colleagues.

Clubbing

  • Gross clubbing is easy to recognize. Early clubbing is more subtle with an impression of fullness and ‘floating’ of the root of the nail bed on compression.

  • The mechanisms that underlie the development of clubbing remain unclear. Possibilities include circulating mediators of vasodilatation released in response to hypoxia, and effects of the vagal nerve resulting from the observation of the association between clubbing and disease in organs with vagal innervation.

  • In children with respiratory symptoms, clubbing usually suggests suppurative lung disease or cyanotic cardiac disease. It can also be seen in children with chronic hypoxaemia from a respiratory cause such as interstitial lung disease (ILD) or bronchiolitis obliterans (BO).

Chest shape

  • Fixed variations of the chest shape are relatively common in children, affecting 0.5% of the population. They usually have no significant functional consequences. The commonest variation is pectus excavatum (see Examining the respiratory system Chapter 40). It is best to avoid the term ‘chest deformity’ in describing normal variations of the chest shape.

  • Hyperinflation (Fig. 1.1) is a reversible change in the chest shape and indicates air trapping, usually as a result of small airways obstruction. In the context of asthma, it suggests poor control. It is most easily seen from the side.

  • Harrison’s sulci (Fig. 1.2) refer to an indentation of the lower chest wall with the apparent splaying of the costal margins. They may be seen in association with hyperinflation. They are associated with chronic respiratory disease associated with increased work of breathing and may be caused by the necessarily increased power of diaphragmatic contraction on relatively soft costal cartilage.

Fig. 1.1 Lateral view of the normal and hyperinflated chest.

Fig. 1.1 Lateral view of the normal and hyperinflated chest.

Fig. 1.2 Anterior views of pectus excavatum and Harrison’s sulci.

Fig. 1.2 Anterior views of pectus excavatum and Harrison’s sulci.

Palpation

  • Placing the hands on the chest can give valuable information about the presence of secretions and wheeze. It can also help determine whether chest expansion is symmetrical.

  • In older children who can perform a vital capacity manoeuvre, measuring the chest expansion, using a tape measure at the level of the xiphoid cartilage, can be predictive of lung volumes measured by spirometry. Depending on the height and sex of the subject, normal values for chest expansion can range from 3 cm to 9 cm.

Percussion

Despite occasional views to the contrary, it is always useful to percuss the chest in children. A dull percussion note is consistent with extensive consolidation or pleural disease, either pleural thickening or pleural fluid.

Stridor

Stridor (from the Latin stridere, to make harsh sounds) is a harsh monophonic noise that comes from the trachea or larynx as a result of narrowing. It may be heard with or without a stethoscope. When the extrathoracic airway is affected, the noise always has an inspiratory component but can be biphasic if the narrowing is severe. When the intrathoracic trachea is affected, the stridor will usually be biphasic, with a relatively loud expiratory phase. A purely inspiratory stridor indicates narrowing of the extrathoracic airway. Stridor is louder when airflows are increased, such as with crying or exertion, and quieter when flows are reduced, e.g. during sleep.

Stertor

This term is used to describe the harsh coarse noises generated by turbulent airflow in the supraglottic space. It may be caused by spasticity of the pharyngeal muscles, e.g. in a child with cerebral palsy, by retained secretions, or by adenotonsillar hypertrophy. Stertor is often louder during sleep, because of reduced tone of the pharyngeal muscles.

Auscultation

A clear description of breath sounds and any added adventitial sounds is much more informative than the often used term ‘air entry’. It is important to listen to all of the lobes of each lung. This means listening at the apices and the axillae, as well as at the front and back of the chest.

Breath sounds

Breath sounds are generated by air moving though the trachea and large bronchi. When listening at the midline over the trachea, the breath sounds are loud, with a full inspiratory and expiratory phase, with the inspiratory phase usually being louder. There is no pause between the two phases. Breath sounds with these characteristics are called bronchial.

  • Vesicular breath sounds. When listening at the periphery of the lung, the breath sounds are quieter, and only the inspiratory phase and the initial part of expiration can be heard. There is a short pause between the two phases.

  • Bronchial breathing. If there is consolidation of the lung, the sound from the large airways passes more easily through the solid material, and bronchial breath sounds are heard at the periphery.

When there is airway narrowing, the expiratory phase of the breath sounds heard at the periphery may become louder and more prolonged. This sign may be present, before an obvious wheeze is heard.

Adventitial noises

  • Wheeze—a whistling ‘musical’ noise, caused by turbulent airflow passing through narrowed medium-sized airways. If present, wheeze always occurs in expiration but may be present on inspiration as well when airways obstruction is severe.

  • Crepitations or crackles—sharp noises, usually heard on inspiration, can be coarse or fine, depending on the pitch and quality of the sound. The mechanism by which the sounds are generated is not well understood. One possibility is that they are caused by fluid clearing rapidly from small airways (coarse) or alveoli (fine) so that pressures on either side of the obstruction suddenly equilibrate, resulting in vibrations of the airway wall. It seems likely that these explanations are rather simplistic. Airflow rapidly diminishes as the airway divides, and gas movement in the bronchioles and alveoli is thought to occur by Brownian motion and diffusion. Such low energy movement cannot produce audible sounds. Whatever the origin of the sound, the presence of crepitations indicates small airway or alveolar disease. When crepitations are present, it is helpful to determine if they are cleared by coughing. This finding suggests that the crepitations are caused by secretions and that chest physiotherapy may be a helpful part of management.

  • Rattles (also known as ruttles)—noises coming from secretions in medium-sized and large airways.

  • Transmitted sounds—noises coming from the upper airway, heard when auscultating the chest.

The terms râles or rhonchi are sometimes used and frequently cause confusion. They were coined by the French inventor of the stethoscope Laennec in the nineteenth century. They mean the same thing—râles is the French word, and rhonchi is Latin. They were used to describe crackles (râle crépitant), rattles (râle sec sonore), and wheeze (râle sibilant). Some doctors still use the terms sibilant and sonorous rhonchi or râles. For the more modern doctor, it is probably best to stick with wheeze, crepitations, and rattles.

Listen to the cough

Some children will cough spontaneously during their clinic visit. Others may be able to do so, if asked. Listening to the nature of the cough can be illuminating.

  • Is it dry or productive-sounding?

  • Is it brassy, croup-like, honking? This type of cough sound originates in the trachea and is consistent with the presence of tracheal narrowing, tracheomalacia, or habit cough.

  • Does it sound effective? Children with neuromuscular weakness may not be able to effectively clear their secretions, putting them at risk of respiratory failure during otherwise trivial viral respiratory tract infections.

Further information

Forgacs P (1978). The functional basis of pulmonary sounds. Chest 73, 399–405.Find this resource:

Lehrer S (2002). Understanding lung sounds (booklet and audio CD). WB Saunders Company, Philadelphia.Find this resource: