Abstract
The history and physical examination in pediatric respiratory medicine remain our most important tools in the evaluation of children presenting with respiratory problems. They guide our differential diagnosis, clinical and investigative approach, and treatments. The global approach to a pediatric respiratory history and physical examination are described and illustrated with the aid of pictures and video in this chapter. Subsequently, approaches to common presentations in Respiratory Medicine including chronic cough, chest pain, dyspnea, cyanosis, noisy breathing, and clubbing are also reviewed.
Keywords
signs and symptoms (respiratory), physical examination, auscultation, respiratory sounds, cough, dyspnea, chest pain, cyanosis, clubbing of digits
In the 21st century, the diagnosis of disease still requires a detailed medical history and a thorough physical examination. For the majority of patients in many areas of the world, additional information from laboratory tests and other data remain rather limited. Modern science and technology have changed the situation considerably in industrialized nations, but we are paying a high price. Cost containment in health care has become essential. Physicians need to be skillful in their history taking and physical examination techniques so they can collect a maximum amount of information before ordering expensive investigations. The relevance of these skills in pediatric respiratory medicine is exemplified by clinical severity scores that are widely used in care maps for asthma, bronchiolitis, and croup, or in scores developed to manage patients suspected to have acute severe respiratory syndromes (e.g., during outbreaks of SARS, H1N1, and other forms of influenza).
The diagnosis of disease in children has to rely on the patient’s history and on observations gathered during the physical examination, even more than in older patients. Young children cannot follow instructions and participate in formal physiologic testing, and physicians hesitate before subjecting their pediatric patients to invasive diagnostic procedures. Diseases of the respiratory tract are among the most common in children, and in the majority of cases they can be correctly identified from medical history data and physical findings alone. The following review of the medical history and physical examination in children with respiratory disease includes some observations that were made with the help of modern technology. These technical aids do not lessen the value of subjective perceptions, but rather emphasize how new methods may further our understanding, sharpen our senses, and thereby advance the art of medical diagnosis.
The History
General Principles
The medical history should be taken in an environment with comfortable seating for all, a place for clothing and belongings, and some toys for younger children. Privacy has to be assured, without the usual interruptions by phone calls and other distractions. If possible, the physician should see one child at a time because the presence of young siblings or other children in the room can be distracting. Data that should be recorded at the beginning include the patient’s name and address, the parents’ or guardians’ home and work phone numbers, the name of the referring physician, and information on the kindergarten or school if this is relevant. In many cases, the history will be given by someone other than the patient, but the physician should still directly ask even young children about their complaints. When asking about the history of the present illness, the physician should encourage a clear and chronological narrative account. Questions should be open-ended, and at intervals the physician should give a verbal summary to confirm and clarify the information. Past medical history and system review are usually obtained by answers to direct questions.
Structure of the Pediatric History
The physician should note the source of and the reason for referral. On occasion, the referral is made by someone other than the patient or the parents (e.g., a teacher, relative, or friend). The physician should identify the chief complaint and the person most concerned about it. The illness at presentation should be documented in detail regarding onset and duration, the environment and circumstances under which it developed, its manifestations and their treatments, and its impact on the patient and family. Symptoms should be defined by their qualitative and quantitative characteristics as well as by their timing, location, aggravating or alleviating factors, and associated manifestations. Relevant past medical and laboratory data should be included in the documentation of the present illness.
This general approach is also applicable when the emphasis is on a single organ system, such as the respiratory tract. The onset of disease may have been gradual (e.g., with some interstitial lung diseases) or sudden (e.g., with foreign body aspiration). The physician should ask about initial manifestations and who noticed them first. The age at first presentation is important, because respiratory diseases that manifest soon after birth are more likely to have been inherited or to be related to congenital malformations. Depending on the duration of symptoms, the illness will be classified as acute, subacute, chronic, or recurrent. These definitions are arbitrary, but diseases of less than 3 weeks’ duration are generally called acute; diseases between 3 weeks’ and 3 months’ duration are subacute; and those that persist longer than 3 months are chronic. If symptoms are clearly discontinuous, with documented intervals of well-being, the disease is recurrent. This distinction is important because many parents may perceive their child as being chronically ill, not realizing that young normal children may have six to eight upper respiratory infections per year, particularly during the first 2 years if the child is in a daycare setting, or if he or she has older siblings.
Respiratory diseases are often affected by environmental factors. There should be a careful search for seasonal changes in symptoms to uncover possible allergic causes. Exposure to noxious inhaled agents, for example, from industrial pollution or more commonly from indoor pollution by cigarette smoke, can sustain or aggravate a patient’s coughing and wheezing. Similarly, a wood-burning stove used for indoor heating may be a contributing factor. The physician should therefore obtain a detailed description of the patient’s home environment. Are there household pets (e.g., dogs, cats, or hamsters) or birds (e.g., budgies, pigeons, or parrots)? What plants are in and around the house? Are there animal or vegetable fibers in the bedclothes or in the floor and window coverings (e.g., wool, feathers)? Are there systems in use for air conditioning and humidification? Is mold visible anywhere in the house?
There may be a relationship between respiratory symptoms and daily activities. Exercise is a common trigger factor for coughing and wheezing in many patients with hyperreactive airways. A walk outside in cold air may have similar effects. Diurnal variation of symptoms may be apparent, and attention should be paid to changes that occur at night. These changes may also be related to airway cooling, or they may reflect conditions that are worse in the recumbent position, such as postnasal drip or gastroesophageal reflux (GER). Food intake may bring on symptoms of respiratory distress when food is aspirated or when food allergies are present.
Many children who present with respiratory symptoms are suffering from infection, most often viral. It is important to know whether other family members or people in regular contact with the patient are also affected. When unusual infections are suspected, questions should be asked about recent travel to areas where exotic organisms may have been acquired. Drug abuse by parents or by older patients and high-risk lifestyles may lead the physician to consider the possibility of acquired immunodeficiency syndrome (AIDS).
Descriptions of respiratory disease manifestations may come from the parents or directly from an older child. Common symptoms are fever, cough and sputum production, wheezing or noisy breathing, dyspnea, and chest pain. Most of these are discussed in more detail later in the chapter.
The past medical history will provide an impression of the general health status of the child. First, the birth history should be reviewed, including prenatal, natal, and neonatal events. The physician should inquire about the course of pregnancy, particularly whether the mother and fetus suffered from infections, metabolic disorders, or exposure to noxious agents (e.g., nicotine). The duration of pregnancy, possible multiple births, and circumstances leading to the onset of labor should be noted. Difficult labor and delivery may cause respiratory problems at birth (e.g., asphyxia and meconium aspiration), and the physician should ask about birth weight and Apgar scores. The physician should carefully review the neonatal course because many events during this period may affect the patient’s respiratory status in later years. Were there any signs of neonatal respiratory distress (e.g., tachypnea, retractions, and cyanosis)? Treatment with oxygen or endotracheal intubation should be recorded. Some extrathoracic disorders provide valuable clues for diagnosis, such as the presence of eczema in atopic infants or neonatal conjunctivitis in an infant with chlamydia pneumonia, particularly if there was a documented infection of the mother.
Much is learned from a detailed feeding history, which should include the amount, type, and schedule of food intake. The physician should ask whether the child was fed by breast or bottle. For the newborn and young infant, feeding is a substantial physical exercise and may lead to distress in the presence of respiratory disease, much as climbing stairs does in the older patient. The question of exercise tolerance in an infant is therefore asked by inquiring how long it takes the patient to finish a feed. The caloric intake of infants with respiratory disease is often reduced despite an increased caloric requirement to support the work of breathing. This reduced caloric intake commonly results in a failure to thrive. Older patients with chronic respiratory disease and productive cough may suffer from a continuous exposure of their taste buds to mucopurulent secretions and may quite understandably lose their appetites, but medical treatment (e.g., with certain antibiotics) may have similar effects. Patients with food hypersensitivity may react with bronchospasm or even with interstitial lung disease on exposure to the allergen (e.g., milk). Physical irritation and inflammation occur if food is aspirated into the respiratory tract. This happens frequently in patients with debilitating neurologic diseases and deficient protective reflexes of the upper airways. However, pulmonary aspiration may also occur in neurologically intact children, and their ethnic background, for example, indigenous people of North America, may suggest an increased risk. A history of cough or choking during feeding should alert the physician to the possibility of pulmonary aspiration.
The physical development of children with chronic respiratory diseases may be retarded. Malnutrition in the presence of increased caloric requirements is common, but the effects of some long-term medical treatments (e.g., steroids) should also be considered. Previous measurements of body growth should be obtained and plotted on appropriate charts. Psychosocial development may be affected if chronic lung diseases (e.g., asthma or cystic fibrosis) limit attendance and performance at school or if behavioral problems arise in children and adolescents subjected to chronic therapy. More severely affected patients may also be delayed in their sexual development.
Many diseases of the respiratory tract in children have a genetic component, either with a clear Mendelian mode of inheritance (e.g., autosomal recessive in cystic fibrosis, homozygous deficiency of α 1 -antitrypsin, X-linked recessive in chronic granulomatous disease, and autosomal dominant in familial interstitial fibrosis) or with a genetic contribution to the cause. Examples of familial aggregation of respiratory disease are chronic bronchitis and bronchiectasis or familial emphysema in patients with heterozygous α 1 -antitrypsin deficiency, in which the susceptibility of the lung to the action of irritants (e.g., cigarette smoke) is increased. A mixed influence of genetic and environmental factors exists in polygenic diseases, such as asthma or allergic rhinitis.
When inquiring about the family history, the physician should review at least two generations on either side. The parents should be asked whether they are related by blood, and information should be obtained about any childhood deaths in the family. The health of the patient’s siblings and also of brothers and sisters of both parents should be documented. Particular attention should be paid to histories of asthma, allergies and hay fever, chronic bronchitis, emphysema, tuberculosis, cystic fibrosis, male infertility, and sudden unexpected infant death.
The physician should obtain a detailed report of prior tests and immunizations. Quite often this requires communication with other health care providers. Results of screening examinations (e.g., tuberculin and other skin tests, chest radiographs, and Cystic Fibrosis newborn screening) should be noted. Similarly, childhood illnesses, immunizations, and possible adverse immunization reactions should be documented. If the history is positive for allergic reactions, these have to be confirmed and defined. Previous hospital admissions and their indications should be listed, and the patient’s current medications and their efficacy should be documented. If possible, the drug containers and prescriptions should be reviewed. The physician may use the opportunity to discuss the pharmacologic information and the technique of drug administration, particularly with inhaled bronchodilator medications.
One of the most important goals in taking a history is to become more aware of the particular psychological and social situation of the patient. It is impossible to judge current complaints or responses to medical interventions without an individual frame of reference for each patient. The physician should encourage the child and the parents to describe a typical day at home, daycare, kindergarten, or school. This will provide valuable information about the impact of the illness on daily routines, the financial implications, the existing or absent social support structures, and the coping strategies of the family. Compliance with medical treatment is rarely better than 50%, and physicians are generally unable to predict how well their patients follow and adhere to therapeutic regimens. Compliance can improve if the patient and the parents gain a better understanding of the disease and its treatment. It is important to recognize prior experiences that the family may have had with the health care system and to understand individual spiritual, religious, and health beliefs. Particularly in children with chronic respiratory ailments whose symptoms are not being controlled or prevented, the effort and unpleasantness (e.g., of chest physiotherapy) may limit the use of such interventions. The physician should also consider the social stigma associated with visible therapy, especially among peers of the adolescent patient.
A review of organ systems is usually the last part of the history and may actually be completed during the physical examination. Although the emphasis is on the respiratory system, questions about the general status of the child will be about appetite, sleep, level of activity, and prevailing mood. Important findings in the region of the head and neck are nasal obstruction and discharge, ear or sinus infection, conjunctival irritation, sore throat, and swallowing difficulty. The respiratory manifestations of coughing, noisy breathing, wheezing, and cyanosis are discussed in detail at the end of this chapter. Cardiovascular findings may include palpitations and dysrhythmia in hypoxic patients; there may be edema formation and peripheral swelling with cor pulmonale. Effects of respiratory disease on the gastrointestinal tract may appear with cough-induced vomiting and abdominal pain. There may be a direct involvement with diarrhea, cramps, and fatty stools in patients with cystic fibrosis. The physician should ask about hematuria and about skin manifestations, such as eczema or rashes, and about swellings and pain of lymph nodes or joints. Finally, neurologic symptoms (e.g., headache, lightheadedness, or paresthesiae) may be related to respiratory disease and cough paroxysms or hyperventilation.
The Physical Examination
Traditionally, the physical examination is divided into inspection, palpation, percussion, and auscultation. The sequence of these steps may be varied depending on the circumstances, particularly in the assessment of the respiratory tract in children. The classic components of the physical examination and some modern aids and additions are discussed in the following sections.
Inspection
Much can be learned from simple observation, particularly during those precious moments of sleep in the young infant or toddler, who when awake can be a challenge even for the skilled examiner. First, the pattern of breathing should be observed. This includes the respiratory rate, rhythm, and effort. The respiratory rate decreases with age and shows its greatest variability in newborns and young infants ( Fig. 1.1A ). Reference values in hospitalized children, excluding those with respiratory disease, show higher values (see Fig. 1.1B ).
The respiratory rate should be counted over at least 1 minute, ideally several times for the calculation of average values. Because respiratory rates differ among sleep states and become even more variable during wakefulness, a note should be made describing the behavioral state of the patient. Observing abdominal movements or listening to breath sounds with the stethoscope placed before the mouth and nose may help in counting respirations in patients with very shallow thoracic excursions.
Longitudinal documentation of the respiratory rate during rest or sleep is important for the follow-up of patients with chronic lung diseases, even more so for those too young for standard pulmonary function tests. Abnormally high breathing frequencies or tachypnea can be seen in patients with decreased compliance of the respiratory system and in those with metabolic acidosis. Other causes of tachypnea are fever (~5–7 breaths/min increase per degree above 37°C), anemia, exertion, intoxication (salicylates), anxiety, and psychogenic hyperventilation. The opposite, an abnormally slow respiratory rate or bradypnea, can occur in patients with metabolic alkalosis or central nervous system depression. The terms hyperpnea and hypopnea refer to abnormally deep or shallow respirations. At given respiratory rates, this determination is a subjective clinical judgment and is not easily quantified unless the pattern is obvious, such as the Kussmaul type of breathing in patients with diabetic ketoacidosis.
Significant changes in the rhythm of breathing occur during the first months of life. Respiratory pauses of less than 6 seconds are common in infants younger than 3 months of age. If these pauses occur in groups of three or more that are separated by less than 20 seconds of respiration, the pattern is referred to as periodic breathing. This pattern is very common in premature infants after the first days of life and may persist until 44 weeks postconceptional age. In full-term infants, periodic breathing is usually observed between 1 week and 2 months of age and is normally absent by 6 months of age. Apnea with cessation of air flow lasting more than 15 seconds is uncommon and may be accompanied by bradycardia and cyanosis. In preterm infants, a drop in oxygen saturation may be seen up to 7 seconds after a respiratory pause when in room air and up to 9 seconds later when on supplemental oxygen.
Other abnormal patterns include Cheyne-Stokes breathing, which occurs as cycles of increasing and decreasing tidal volumes separated by apnea (e.g., in children with congestive heart failure or increased intracranial pressure). Biot breathing consists of irregular cycles of respiration at variable tidal volumes interrupted by apnea and is an ominous finding in patients with severe brain damage.
After noting the rate and rhythm of breathing, the physician should look for signs of increased respiratory effort. The older child will be able to communicate the subjective experience of difficult breathing, or dyspnea. Objective signs that reflect distressed breathing are chest wall retractions, visible use of accessory muscles and the alae nasi, orthopnea, and paradoxical respiratory movements. The more negative intrapleural pressure during inspiration against a high airway resistance leads to retraction of the pliable portions of the chest wall, including the intercostal and subcostal tissues and the supraclavicular and suprasternal fossae. Conversely, bulging of intercostal spaces may be seen when pleural pressure becomes greatly positive during a maximally forced expiration. Retractions are more easily visible in the newborn infant, in whom intercostal tissues are thinner and more compliant than in the older child.
Visible contraction of the sternocleidomastoid muscles and indrawing of supraclavicular fossae during inspiration are among the most reliable clinical signs of airway obstruction. In young infants, these muscular contractions may lead to head bobbing, which is best observed when the child rests with the head supported slightly at the suboccipital area. If no other signs of respiratory distress are present in an infant with head bobbing, however, central nervous system disorders, such as third ventricular cysts with hydrocephalus, should be considered. Older patients with chronic airway obstruction and extensive use of accessory muscles may appear to have a short neck because of hunched shoulders. Orthopnea exists when the patient is unable to tolerate a recumbent position, for example, with severely increased upper airway resistance and obstruction during sleep.
Flaring of the alae nasi is a sensitive sign of respiratory distress and may be present when inspiration is abnormally short (e.g., under conditions of chest pain). Nasal flaring enlarges the anterior nasal passages and reduces upper and total airway resistance. It may also help to stabilize the upper airways by preventing large negative pharyngeal pressures during inspiration.
The normal movement of chest and abdominal walls is directed outward during inspiration. Inward motion of the chest wall during inspiration is called paradoxical breathing. This is seen when the thoracic cage loses its stability and becomes distorted by the action of the diaphragm. Classically, paradoxical breathing with a seesaw type of thoracoabdominal motion is seen in patients with paralysis of the intercostal muscles, but it is also commonly seen in premature and newborn infants who have a very compliant rib cage. Inspiratory indrawing of the lateral chest is known as Hoover sign and can be observed in patients with obstructive airway disease. Paradoxical breathing also occurs during sleep in patients with upper airway obstruction. The development of paradoxical breathing in an awake, nonparalyzed patient beyond the newborn period usually indicates respiratory muscle fatigue and impending respiratory failure.
Following inspection of the breathing pattern, the examiner should pay attention to the symmetry of respiratory chest excursions. Unilateral diseases affecting lungs, pleura, chest wall, or diaphragm may all result in asymmetric breathing movements. Trauma to the rib cage may cause fractures and a “flail chest” that shows local paradoxical movement. Pain during respiration usually leads to “splinting” with flexion of the trunk toward and decreased respiratory movements of the affected side. The signs of hemidiaphragmatic paralysis may be subtle. In complete unilateral paralysis, there may be a shift in the epigastric abdominal wall during deep inspiration diagonally toward the side of the lesion and upward. This may be more noticeable in the lateral decubitus position with the paralyzed diaphragm placed up, a position that tends to accentuate a paradoxical inward epigastric motion on the affected side.
Other methods to augment inspection of chest wall motion use optical markers. In practice, this technique is done by placing both hands on either side of the patient’s lateral rib cage with the thumbs along the costal margins. Divergence of the thumbs during expansion of the thorax supposedly aids in the visual perception of the range and symmetry of respiratory movements. This technique is of little use in children. A more accurate method of documenting the vectors of movement at different sites (but one that is not yet practical for bedside evaluation) is to place a grid of optical markers on the chest surface and film their positional changes during respiration relative to a steady reference frame. A similar concept is used in optical studies of chest deformities. Projection of raster lines onto the anterior chest surface allows stereographic measurement of deformities, such as pectus excavatum, and augments the visual image of the surface shape ( Fig. 1.2 ). In practice and without such tools, however, the physician should inspect the chest at different angles of illumination to enhance the visual perception of chest wall deformities. Their location, size, symmetry, and change with respiratory or cardiac movements should be noted.
The physician should measure the dimensions of the chest. Chest size and shape are influenced by ethnic and geographic factors that should be taken into account when measurements are compared with normative data. Andean children who live at high altitudes, for example, have larger chest dimensions relative to stature than children in North America. The chest circumference is usually taken at the mammillary level during midinspiration. In practice, mean readings during inspiration and expiration should be noted ( Fig. 1.3A ). Premature infants have a greater head circumference than chest circumference, while these measurements are very similar at term (see Fig. 1.3B ). Malnutrition can delay the time at which chest circumference begins to exceed head circumference.
Further objective documentation of the chest configuration may include measurements of thoracic depth (anteroposterior [AP] diameter) and width (transverse diameter). The thoracic index, or the ratio of AP over transverse diameter, is close to unity in infants and decreases during childhood. Measurements should be taken with a caliper at the level of the nipples in upright subjects. Normative values for young children are available but dated ( Fig. 1.4 ). Most of the configurational change of the chest occurs during the first 2 years and is probably influenced by gravitational forces after the upright position becomes common. Disease-related changes in thoracic dimensions occur either as potential causative factors (e.g., the elongated thorax with a stress distribution that favors spontaneous pneumothorax in lanky adolescents, particularly males who increase their thoracic height versus width more than females) or as a secondary event (e.g., the barrel-shaped chest in patients with emphysema and chronic hyperinflation of the lung).
Inspection of the patient should also be directed to the extrathoracic regions. Many observations on the examination of the head and neck provide valuable clues to the physical diagnosis. Bluish coloration of the lower eyelid (“allergic shiners”); a bilateral fold of skin just below the lower eyelid (Dennie lines); and a transverse crease from “allergic salutes,” running at the junction of the cartilaginous and bony portion of the nose, may all be found in atopic individuals. The physician should always examine the nose and document bilateral patency by occluding each side while feeling and listening for air flow through the other nostril. Even without a speculum, one can assess the anterior half by raising the nose tip with one thumb and shining a light into the nasal passageways. Color and size of the mucosa should be noted. The frequency of asymptomatic nasal polyps seems to be high. Most polyps arise from the mucosa of the ostia, clefts, and recesses in the ostiomeatal complex and have the appearance of white gelatinous grapes. Easily visible nasal polyps are common in patients with cystic fibrosis. Nasal polyposis may also be familial or associated with allergy, asthma, and aspirin intolerance.
The oropharynx should be inspected for its size and signs of malformation, such as cleft palate, and for signs of obstruction by enlarged tonsils. Evidence of chronic ear infections should be documented, and the areas over frontal and maxillary paranasal sinuses should be tested for tenderness. Inspection of the skin is important and may reveal the eczema of atopy. The finding of a scar that typically develops at the site of a successful bacillus Calmette-Guérin (BCG) vaccination may be relevant. In North American children, these scars are usually found over the left deltoid, but other sites, including buttocks and lower extremities, are also used for BCG inoculation in different parts of the world. Common physical findings such as cyanosis, clubbing, and the cardiovascular signs of pulmonary disease are discussed in more detail at the end of this chapter .
Palpation
Palpation follows chest inspection to confirm observed abnormalities, such as swellings and deformations; to identify areas of tenderness or lymph node enlargement; to document the position of the trachea; to assess respiratory excursions; and to detect changes in the transmission of voice sounds through the chest. Chest palpation may offer the first physical contact with the patient, and it is very important for the physician to perform this procedure with warm hands.
Palpation should be done in an orderly sequence. Commonly, one begins with an examination of the head and neck. Cervical lymphadenopathy and tenderness over paranasal sinuses should be noted. Palpation of the oropharynx may be indicated to find malformations such as submucosal clefts or to identify causes of upper airway obstruction. The position of the trachea must be documented in every patient. This is a very important part of the physical chest examination because tracheal deviation most often indicates significant intrathoracic or extrathoracic abnormalities.
In the older child, the tracheal position is assessed by placing the index and ring fingers on both sternal attachments of the sternocleidomastoid muscles. The trachea is then felt between these landmarks with the middle finger on the suprasternal notch. In small children, palpation is done with one index finger sliding gently inward over the suprasternal notch. Looking for asymmetry, the physician should always make sure that the patient is in a straight position, and deformities (e.g., scoliosis) should be taken into account.
A very slight deviation of the trachea toward the right is normal. Marked deviations may indicate a pulling force toward the side of displacement (e.g., atelectasis) or a pushing force on the contralateral side (e.g., pneumothorax). The physician should note whether the displacement is fixed or whether there is a pendular movement of the trachea during inspiration and expiration that may suggest obstruction of a large bronchus. Posterior displacement of the trachea may occur with anterior mediastinal tumors or barrel chest deformities, whereas an easily palpable anteriorly displaced trachea is sometimes seen with mediastinitis. In patients with airway obstruction and respiratory distress, retractions of the suprasternal fossa may be seen, and a “tracheal tug” may be felt by the examiner.
Placing the hands on both sides of the lateral rib cage, the physician should feel for symmetry of chest expansion during regular and deep breathing maneuvers. Slight compression of the chest in the transverse and AP directions may help to localize pain from lesions of the bony structures. Voice-generated vibrations are best felt with the palms of both hands just below the base of the fingers placed over corresponding sites on the right and left hemithorax. Asymmetric transmission usually indicates unilateral intrathoracic abnormalities. The patient is asked to produce low-frequency vibrations of sufficient amplitude by saying “ninety-nine” in a loud voice. In young infants, crying may produce the vibrations that are felt as tactile fremitus over the chest wall. This fremitus is decreased if an accumulation of air or fluid in the pleural space reduces transmission. Small consolidations of the underlying lung will not diminish the tactile fremitus as long as the airways remain open, whereas collapse of the airways and atelectasis will reduce the transmission of vibratory energy if larger portions of the lung are affected.
Percussion
Percussion is used to set tissues into vibration with an impulsive force so that their mechanical and acoustic response can be studied. If the vibrations are not damped and continue for a significant amount of time, the perceived sound will be resonant or “tympanic,” whereas rapid attenuation of the vibrations will lead to a flat or “dull” percussion note. The former occurs when there is a large acoustic mismatch (e.g., tissue overlying an air-filled cavity), whereas the latter occurs when the underlying tissue is similar to the surface tissue and vibratory energy propagates away quickly. Structures that absorb energy when struck by a sound at their natural frequency continue vibrating after the initial sound is gone and are called resonant. The fundamental resonance of the thorax depends on body size and is about 125 Hz for adult males, between 150 and 175 Hz for adult females, and between 300 and 400 Hz for small children.
Chest percussion in children is performed by light tapping with the middle finger (the plexor) on the middle or terminal phalanx of the other hand’s middle finger (the pleximeter). The pleximeter should be placed firmly but not hard, and care should be taken that other fingers do not touch the chest wall, which may cause artificial damping of the percussion note. Percussion should be gentle, with quick perpendicular movements of the plexor originating from the wrist ( Fig. 1.5 ). The patient should be relaxed during the examination because tension of the chest wall muscles may alter the percussion note. More importantly, chest deformities and scoliosis in particular will have a significant effect on percussion findings.
Symmetric sites over the anterior, lateral, and posterior surface of the chest should be compared in an orderly fashion. As with chest auscultation, findings should be reported with reference to standard external anatomic landmarks ( Fig. 1.6 ). The ribs and vertebral spinous processes are used for horizontal mapping. The level at which the tympanic lung resonance changes to a dull percussion note should be defined over the posterior chest during maximal inspiration and expiration to delineate the lung borders and their respiratory excursions.
Subjective assessment of percussion note differences includes both acoustic and tactile perception. Tympanic, lower-pitched percussion notes mean less-damped vibrations of longer duration, which are felt by the pleximeter finger and heard by the examiner. These resonant sounds can be exaggerated, or hyperresonant, over hyperinflated lungs but also in some otherwise healthy thin individuals. Observer agreement on this sign is relatively poor unless the finding is unilateral.
Dull sounds with higher frequencies correspond to vibrations that die away quickly. Dullness replaces the normal chest percussion note when fluid accumulates in the pleural space or when consolidation occurs in the underlying pulmonary parenchyma close to the chest wall. Similar to the vibrations generated by percussion, the vibrations from the patient’s voice (“say ‘ninety-nine’ ”) will also not be felt under these circumstances. The tactile fremitus is equally absent over areas of pneumothorax, whereas percussion, as noted above, should have a hyperresonant quality.
Conventional percussion cannot detect small pulmonary lesions located deeply within the thorax. Auscultatory percussion has been proposed to overcome this limitation. This technique combines light percussion of the sternum with simultaneous auscultation over the posterior chest. A decrease in sound intensity is believed to indicate lung disease. The method is of little value, however, because even large intrathoracic lesions can remain undetected since percussion sounds may either be totally absorbed within the lung or may travel as transverse waves along the thoracic bones.
Auscultation
Auscultation is arguably the most important part of the physical chest examination. The subjective perception of respiratory acoustic signs is influenced by the site and mode of sound production; by the modification of sound on its passage through the lung, chest wall, and stethoscope; and, finally, by the auditory system of the examiner. Knowledge about these factors is necessary to appreciate fully the wealth of information that is contained in the acoustic signs of the thorax.
Thoracic Acoustics
Observations on sound generation in airway models and electronic analyses of respiratory sounds suggest a predominant origin from complex turbulences within the central airways. The tracheal breath sound heard above the suprasternal notch is a relatively broad-spectrum noise, ranging in frequency from less than 100 Hz to greater than 2000 Hz. Resonances from the trachea and from supraglottic airways “color” the sound ( Fig. 1.7 ). The lengthening of the trachea with growth during childhood causes lower tracheal resonance frequencies. A dominant source of tracheal breath sounds is turbulence from the jet flow at the glottic aperture. However, narrow segments of the supraglottic passages also contribute to sound generation. There is a very close relationship between air flow and tracheal sound intensity, particularly at high frequencies. In the presence of local narrowing (e.g., in children with subglottic stenosis), flow velocity at the stenotic site is increased, and so is the tracheal sound intensity. Relating tracheal sound levels to air flow measured at the mouth can provide information about changes during therapy. Auscultation over the trachea will provide some information under these circumstances, but objective acoustic measurements are required for accurate comparisons.
Basic “normal” lung sounds heard at the chest surface are lower in frequency than tracheal sounds because sound energy is lost during passage though the lungs, particularly at higher frequencies. However, lung sounds extend to frequencies higher than traditionally recognized. More recent observations on the effects of gas density indicate that lung sounds at frequencies above 400 Hz are mostly generated by flow turbulence. At lower frequencies, other mechanisms that are not directly related to air flow (e.g., muscle noise and thoracic cavity resonances) have prominent effects on lung sounds, and gas density effects are less obvious. Inspiratory lung sounds show little contribution of noise generated at the glottis. Their origin is likely more peripheral (i.e., in the main and segmental bronchi). Expiratory lung sounds appear to have a central origin and are probably affected by flow convergence at airway bifurcations ( Fig. 1.8 ).
Sound at different frequencies takes different pathways on the passage through the lung. Low-frequency sound waves propagate from central airways through the lung parenchyma to the chest wall. At higher frequencies, the airway walls become effectively more rigid and sound travels further down into the airways before it propagates through lung tissue. This information cannot be gathered on subjective auscultation but requires objective acoustic measurements. A trained ear, however, will recognize many of the findings that are related to these mechanisms. For example, lung sounds in healthy children and adults are not necessarily equal at corresponding sites over both lungs. In fact, expiratory sounds are typically louder at the right upper lobe compared with the left side. Similar asymmetry has been recognized when sound is introduced at the mouth and measured at the chest surface. A likely explanation for this asymmetry is the effect on sound propagation by the cardiovascular and mediastinal structures to the left of the trachea. Asymmetry of lung sounds is also noticeable in most healthy subjects during inspiration when one listens over the posterior lower chest. The left side tends to be louder here, probably because of the size and spatial orientation of the larger airways due to the heart.
Objective acoustic measurements have also helped to clarify the difference between lung sounds in newborn infants and in older children. The most obvious divergence occurs in lung sounds at low frequencies where newborn infants have much less intensity. This may be explained by thoracic and airway resonances at higher frequencies in newborn infants and perhaps also by their lower muscle mass. Lung sounds at higher frequencies are similar between newborn infants and older children ( Fig. 1.9 ).
