The aim of the physical examination of the respiratory system is to establish (a) pathology of the disease like collapse, consolidation, cavity, etc.; (b) the anatomical site of the disease, i.e. which lobe and side of the lung is involved, and (c) the possible etiology (tuberculosis, bronchogenic carcinoma, etc.) responsible for this. To achieve this, the golden rule of inspection, palpation, percussion and auscultation of the chest is to be followed in a systematic manner.
General physical examination findings pertinent to the respiratory system are as follows.
(a) Emaciation
Loss of subcutaneous fat and altered subcostal angulations are seen in patients of advanced pulmonary tuberculosis, acquired immunodeficiency syndrome, malabsorption syndrome, lung cancer and emphysema. On the other hand, apparent weight gain is noticed in cases of cor pulmonale leading on to cardiac failure. Patients of superior vena caval (SVC) obstruction will have swollen face and bloated upper half of the body. Chronic steroid therapy will also produce weight gain.
(b) Anemia
Patients of pulmonary tuberculosis, lung cancer, other malignancies, chronic renal failure, various infiltrative disorder of the bone marrow, suppurative lung diseases, poor nutrition and those with continued hemoptysis will have anemia of various degrees. On the other hand, suffused conjunctivae are common in secondary polycythemia and in superior vena caval obstruction.
(c) Lymphadenopathy
Generalized lymphadenopathy is usually a feature of tubercular lymphadenitis although the cervical group of lymph nodes are commonly affected. Other causes of generalized lymphadenopathy are: lymphomas, leukemia, HIV infection, sarcoidosis and fungal infections. Metastatic lymph nodes secondary to bronchogenic carcinoma are usually single and hard to feel on palpation and the supraclavicular lymph nodes are the commonest ones to be involved although other cervical nodes may also be affected. Axillary and inguinal lymphadenopathy secondary to lung cancer is very unusual.
(d) Jugular Venous Pressure
Raised jugular venous pressure is common in right-sided heart failure secondary to cor pulmonale and in pericardial effusion. The jugular vein along with other neck veins are engorged and nonpulsatile in SVC obstruction. A pulsus paradoxus of more than 10 mm Hg is seen in patients of acute exacerbations of COPD and in acute bronchial asthma. In the latter, it is an indicator of severe asthma.
(e) Edema
This is an evidence of either right-sided heart failure or hypoproteinemia due to poor intake, excessive loss in sputum in suppurative lung diseases and loss by the kidneys involved in secondary amyloidosis due to bronchiectasis, chronic empyema or long standing pulmonary tuberculosis.
This is a bluish discoloration of the skin and mucous membrane due to an increase in the amount of reduced hemoglobin in the capillary blood (in excess of 5 gm/100 ml). It is the absolute amount of reduced hemoglobin rather than the relative amount which is important for the development of cyanosis. Thus, in severe anemia when the total hemoglobin is low (consequently the total reduced Hb), detection of cyanosis is difficult even if there is marked arterial desaturation. Presence of clinical cyanosis in severe anemia is a very serious situation. On the other hand, higher the hemoglobin greater is the tendency towards 2cyanosis. Thus, patients with polycythemia tend to be cyanotic at higher levels of arterial saturation. Cyanosis is most marked in the oral mucosa, lips, and undersurface of the tongue, nail beds, ears, malar eminences and the conjunctivae. The accurate detection of cyanosis may not be easy always. In some, it can be detected when the oxygen saturation drops down to 85 percent and in others it may not be detected until the saturation falls below 75 percent. The other way of cyanosis being produced, is through high extraction of oxygen in an otherwise normally saturated blood. Thus, cyanosis can be divided into 2 types: central, and peripheral. In the former, either the saturation of oxygen is low or abnormal hemoglobin is present in the blood. In the peripheral type, the saturation is normal but there is slowing of blood flow or there is higher extraction of oxygen from blood. In this type, the mucous membranes of the lips and tongue are spared. Some of the causes of cyanosis are shown in Table 1.1 below.3,4
There are certain situations when there is severe hypoxemia but no cyanosis will be detected on clinical examination. They are: severe anemia, carbon monoxide poisoning (because carboxyhemoglobin imparts a cherry red color), fever with peripheral vasodilatation (high capillary blood flow reduces oxygen extraction and minimizes cyanosis) and cosmetics, which may sometimes mask the presence of cyanosis. Pulmonary edema with cardiogenic shock will produce both central and peripheral types of cyanosis. Patent ductus arteriosus with reversed shunt will produce differential cyanosis (cyanosis in lower limbs but not in the upper). Some other causes of cyanosis due to hypoxemia is shown in Table 1.2.5
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(g) Clubbing and Hypertrophic Pulmonary Osteoarthropathy (HPOA)
Hippocrates first described clubbing more than 2.500 years ago. It may be seen alone or as part of an entity called hypertrophic osteoarthropathy, which include periostitis, arthritis and sometimes thickening, and edema of the skin around the affected joints (Figs 1.1 and 1.2). Clubbing is the painless uniform swelling of the terminal phalanges of the digits.6–11
Pulmonary diseases such as cancer, abscess, empyema, bronchiectasis and cystic fibrosis are the major diseases known to be associated with hypertrophic osteoarthropathy. Digestive tract cancer and cyanotic congenital heart diseases are well known association (details in Table 1.3).
Diagnosis of clubbing in its early stage is difficult and a lot of inter observer variations do exist.
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The earliest signs described variously are as follows:
- Profile sign. Profile angle is constituted between a point in the distal digital crease, Datum point (cuticle or junction point between the nail and the skin) and a point at l/3rd of the distance from the cuticle to the fingertip. Normally the angle is less than 160–180 degrees and is increased in clubbing.
- Hyponychial angle. This angle is constructed between a point on the distal digital crease, Datum point and the hyponychium (thickened stratum corneum lying under the free edge of nail). It is normally up to 188 degrees and is increased in clubbing. This angle is best constructed by means of a shadowgram.
Other less sensitive indicators of early clubbing are:
- An increase in the volume of the finger tip (normally up to 56% and measured by a plethysmograph) and
- An increase in the longitudinal curvature of the nail (normal 8–10 diopters).
The increase in the volume of the clubbed fingers is due to an increase in the vascular connective tissues as seen in cases of congenital cyanotic heart diseases. Many theories have attempted to explain the appearance of this sign but few have persisted. There is no accepted unified theory of the mechanism of clubbing. Obviously they will be different in different conditions. The proposed theories are: circulation of vasodilators (carbonic acid, ferritin, prostaglandins, bradykinin, 5-hydroxytryptamine and adenine nucleotides); tissue hypoxemia; neural mechanisms and genetic factors. The usual causes of clubbing are summarized in Table 1.3. Hypertrophic pulmonary osteoarthropathy affects bones and joints and is characterized by radiological signs of subperiosteal bone formation, bone pain, ankle edema, joint pain, stiffness and synovial effusion. This condition should be differentiated from hypervitaminoses A and D and fluorine toxicity where new bone formation does not occur. Clubbing occurs in about 90 percent of cases of HPOA and is usually very gross. Although HPOA can occur without clubbing, some think that the later is an essential component. Even if clubbing and HPOA have many causes in common, the prevalence differs. While clubbing is universal in congenital cyanotic heart diseases, it is common in primary biliary cirrhosis, cryptogenic fibrosing alveolitis and subacute bacterial endocarditis, HPOA is distinctly uncommon in these conditions. Proposed mechanisms of HPOA are: circulation of bioactive compounds (osteoblast stimulating factor); tissue hypoxemia; immunologic mechanisms; hormonal factors (growth hormone, altered estrogen metabolism, long acting thyroid stimulating substance-LATS and parathormone); neural mechanisms and genetic factors.12,134
Even some other findings other than those mentioned earlier will provide important clues (Fig. 1.3).
After the general physical examination, one should proceed to examine various systems.
The examination of the respiratory system will be described here in detail. One must not forget to examine the upper respiratory tract. This is the area above the trachea and can provide important clues to some diseases. The pale nasal mucosa with polyps is frequently found in cases of bronchial asthma. Short neck, hypertrophic turbinates, enlarged tonsils, adenoids and uvula, and macroglossia may be the cause of upper airways obstruction leading on to obstructive sleep apnea. Poor orodental hygiene may be the cause of aspiration pneumonias and lung abscess. Nasal ulcers may be seen in vasculitis.
EXAMINATION OF THE CHEST
For descriptive purposes, various areas of the chest are: supraclavicular, infraclavicular, mammary, inframammary, axillary (supra-, mid-, and infra-), suprascapular, interscapular, and infrascapular. The chest examination should be divided into inspection, palpation, percussion and auscultation.
Inspection
One should stand at the foot end of the bed and observe the patient. The respiratory rate varies from 14 to 18 per minute in normal healthy adults and is thoracoabdominal type. An increase in the rate of respiration (tachypnea) is common in many respiratory diseases including pneumonias, bronchial asthma in the acute phase, acute attacks of chronic bronchitis and emphysema, interstitial lung disease, acute respiratory distress syndrome and with many other nonrespiratory diseases. The general look of the patient like emaciation (discussed above) blue and bloated appearance (chronic bronchitis in failure), pursed lip breathing (emphysema), toxic and sick look (pneumonia and septicemia), painful catchy breathing with a fixed and immobile chest wall (pleurisy), swollen face and upper extremities (superior vena caval obstruction) audible stridor (upper airways obstruction) and wheezing (bronchial asthma) are few important observations which may give clues to the possible diagnosis. Excursion of the accessory muscles of respiration will indicate that the patient is in respiratory distress. Symmetry of the chest wall then should be looked for and is to be compared region wise on both sides. Retraction of the chest wall will mean loss of lung volume, which may be due to collapse, fibrosis or pleural thickening. Other signs of volume loss may be a drooping of the shoulder on the same side, a deformed spine with concavity towards the affected side and a lowered nipple position especially in the male. A prominent or a bulging chest wall on the other hand may be due to pleural effusion, pneumothorax or a space-occupying lesion. In either case the movement of the chest wall will be decreased. A winged scapula (scapular sign) is seen in serratus anterior muscle paralysis. Any abnormal engorged veins in the chest wall should be noted with their directions of blood flow. Puncture or biopsy mark and chest tube, if any, should provide important diagnostic clues. Paradoxical movement of the diaphragm during respiration may be present in cases of paralysis of the phrenic nerve, commonly due to bronchogenic carcinoma. Sometimes a prominent sternocleidomastoid may be apparent and will indicate the tracheal shift to the side of prominence (Trail sign).
Palpation
Position of the trachea is to be ascertained first during palpation and then localized tenderness (secondary deposits or pleurisy) should be looked for. Some of the other findings of inspection including movements are to be confirmed. Vocal fremitus is to be compared on identical areas on both sides. Vocal fremitus will be decreased in conditions like pleural effusion, pleural thickening, pneumothorax, collapse and fibrosis. Consolidation and a large cavity in communication with a bronchus will increase the vocal fremitus. Displacement of the apex beat will be due to a loss of lung volume (shift to the same side). Pleural effusion, pneumothorax, 5and conditions of space occupying lesions will shift the apex beat to the other side. On occasions, one may be able to palpate coarse crepitations (friction crepitus) and pleural rub (friction fremitus).
Percussion
The rules of percussion are: (i) Percussing finger should strike the pleximeter finger perpendicularly with the movement being from the wrist joint and should be immediately lifted up from the pleximeter. The force of percussion should be light/heavy enough (according to the area percussed and built of the patient) to just elicit the note. (ii) Percussion should be from a normal to an abnormal area or from a resonant to a less resonant area. (iii) Identical areas on both sides are to be compared. (iv) Percussion should be parallel to the border/organ to be percussed. Impaired percussion note is present in conditions like pleural effusion (note is often stony dull), pleural thickening, collapse, and fibrosis. The dullness in pleural effusion will have a rising level and it will shift (shifting dullness) unless it is loculated or the effusion is massive. Hyperresonant note is due to pneumothorax and sometimes due to a large and superficial cavity containing air or large bullae. Coin test will be positive in case of pneumothorax. If a hydropneumothorax is present, a horizontal level of dullness will be there due to fluid and above that, the area will be hyperresonant due to air. The dullness will also shift. In such cases one may hear a succussion splash. However, stomach containing fluid and air and a large cavity with fluid and air may also produce succussion splash. The levels of both the diaphragms and the cardiac borders (cardiac dullness) are to be delineated during this step of examination. Normally the lower level of the right diaphragm lies in the 6th, 8th and 10th intercostal spaces anteriorly, in the mid axillary line and in the midscapular lines respectively and the left one is about one space lower than the right. The diaphragms can move two spaces or more during respiration (usually 1 cm in normal tidal breathing but may be up to 10 cm on forced excursion). In emphysema the cardiac dullness will be obliterated and both the diaphragms lie low and are flat. The cardiac dullness may be enlarged due to pericardial effusion. The diaphragm will be placed higher than the normal positions either due to phrenic nerve palsy or injury, or be pulled up due to loss of lung volume. It may also be pushed up due to intra-abdominal causes like ascites. To differentiate between the cause of a high diaphragm due to phrenic nerve palsy and ascites, one has to do a tidal percussion to see the movement of the diaphragm during respiration. The movement will be absent or moves up rather than down during inspiration in case of phrenic nerve palsy but will be present if pushed up due to ascites.
Auscultation
In auscultation one should describe the nature and intensity of breath sounds, presence of adventitious sounds and the character of the vocal resonance. Normally the breath sounds are vesicular in character. This is defined as the passage of air through normal alveoli and is characterized by the inspiratory phase being longer than the expiratory phase. The last part of the expiration is not heard and there will be no gap between the two phases. Except over the trachea and a small area surrounding it, the breath sound is vesicular all over the chest. Bronchial breath sounds are due to the passage of air through the trachea and major bronchi. The most important characteristic of this sound is the hollow or aspirating character of the expiratory phase. The expiratory phase is longer or at least as long as the inspiratory phase and there will be a gap between the two-phases. The bronchial breath sound may be high-pitched or low pitched. High-pitched bronchial breath sound (tubular) is heard over an area of consolidation, collapse with a patent bronchus and over a tense pleural effusion. In the latter, the collapsed and floating lung behaves like a solid area and therefore one can hear the bronchial breathing above and medial to the pleural effusion. Low-pitched bronchial sound is heard over a cavity (a narrow opening with sudden enlargement-cavernous type). When this has a metallic overtone, it is called an amphoric breath sound. This is heard over a large superficial cavity, bronchopleural fistula and in pneumothorax with bronchial communication. In chronic obstructive airways disease, the expiratory phase may be prolonged without the change of the normal vesicular character. Intensity of the breath sound is diminished in collapse, fibrosis, pleural thickening, pleural effusion and pneumothorax. In the latter two conditions, the breath sound may be totally absent on auscultation. In interstitial fibrosis the intensity sometimes appears to be increased when the bronchi are closer to the chest wall because of the intervening interstitial and alveolar fibrosis. Adventitious sound are either rhonchi or crepitations or pleural rub. Rhonchi are musical and continuous sounds produced by the passage of air through narrowed segments of bronchi either due to bronchospasm, edema, mucus plugging or stenosis. Although there is no established criteria, these continuous sounds usually last for more than 0.25 seconds. These sounds are called sibilant rhonchi 6(wheeze) when they are high pitched and their dominant frequency is 400 Hz or more. They are more like a hissing sound. On the other hand low pitched continuous sound is more like a snoring sound and the dominant frequency is about 200 Hz or less and is called as sonorous rhonchi. While the sibilant and sonorous rhonchi are called as wheeze and rhonchus (American Thoracic Society recommendation), the British usage is high pitched and low-pitched wheeze respectively. On the other hand Laennec had called all types of adventitious sounds as rales. The usual causes are bronchial asthma, chronic bronchitis, pulmonary edema and localized obstruction (tumor and foreign body). Aspirations and pulmonary embolism may also produce rhonchi. High-pitched continuous sounds are associated with narrowing of the central airways, such as bronchospasm, edema of the airway lining, mucous plugging, and foreign bodies or tumor. When the high-pitched continuous sound is confined to inspiration or accentuated during inspiration, it is called stridor. This is a common correlate of a large airway obstruction. Lower pitched continuous sounds are usually associated with secretions in the airways and are changed markedly after cough and expectoration. Crepitations are discontinuous sounds produced by sudden opening of collapsed alveoli or due to air being passed through fluid. These sounds occur in brief bursts similar to the popping sounds of bubbles or the crackling sounds of a fire. Alternatively, they are called as crackles or rales. They are further divided into coarse and fine. Coarse crepitations are louder, lower pitched and slightly longer in duration than fine crackles. Interstitial lung diseases, early congestive cardiac failure, consolidation and fibrosis will produce fine crepitations and bronchiectasis and pulmonary edema will produce coarse crepitations. Crepitations in chronic bronchitis are either fine or coarse. Continuous sounds usually reflect abnormalities of the airways; and discontinuous sounds those of the parenchyma and /or the airways. Pleural rub has a grating or leathery character and is phasic with respiration being heard both in inspiration and expiration. It does not change with cough as may occur with crepitations and is better heard if the stethoscope is pressed firmly against the chest wall. It is usually present in pleurisy during active inflammation or even in pleural thickening if the two pleural surfaces rub against each other. Vocal resonance is the auscultatory counterpart of vocal frernitus and is more accurate than the latter. Aegophony is a characteristic sound heard like a nasal twang when the patient says one-two-three. Bronchophony is a still clearer form of vocal resonance. Whispering pectoriloquy the clear audibility of whispering sounds. All these three forms of sounds are different grades of vocal resonance and are usually heard in areas of consolidation or where one gets a bronchial breath sound. In cases of COPD, one has to note forced expiratory time (FET). The patient is asked to take a deep inspiration and then to expire as forcefully and as quickly as possible and the expiration time is noted with the stethoscope kept over the trachea. Normally this is 3 to 4 seconds and, if it exceeds 6 seconds, it indicates significant amount of airways obstruction. This roughly corresponds to a FEV1/FVC of less than 65 percent.
Vesicular sound has a frequency content that is maximal between 100 and 300 Hz, with little energy content over 500 Hz and has a lower pitch. In most of the conducting airways gas flow is laminar and in the larger airways it is turbulent. The vibrations of the gas in the large airways are transmitted to the walls of the airways and thence to the surface of the chest and also as airborne sound towards the mouth and the periphery. As the sound travels towards the periphery and chest wall, it progressively gets filtered and attenuated. By filtration, components of sound occurring at different frequencies or pitches are transmitted differently. The transmission path acts as a low pass filter preferentially passing low frequency sounds.
Bronchial breathing contains a wide range of frequencies extending from the threshold of audibility to more than 1000 Hz. When the transmission path to the surface of the chest is altered as in consolidation, the filtering effect is decreased so that the sound over the lung fields in the periphery is same as that over the large airways. This is accompanied by alterations in the transmission of voiced sounds, which are heard more clearly over regions of consolidation (increased VR).
There is still controversy regarding the site of generation of sound. Some believe that sound is generated in the periphery.
Adventitious sounds17,18 are believed to result from abnormal motions of airway walls or materials within the airways during breathing. In contrast, normal sounds result largely from vibrations within the gas itself. Continuous sounds (rhonchi) are generated by a regular vibration or oscillation of the airway wall at one or more sites drawing energy from the airflow. The pitch of a wheeze is independent of gas density. These sounds are produced when air passing through a narrowed airway at high velocity produces a decrease in the gas pressure in the airway at the region of constriction (Bernoulli's 7principle). If allowed by the other forces acting on the airway, collapse will continue progressively until there is a substantial resistance and the flow is decreased. Then the internal pressure increases and the lumen enlarges. This alternation of the wall between almost closed and almost open can continue as long as flow rate is high enough. Crepitations are discrete vibrations that result from the sudden release of energy stored in elastic or surface forces within the lung. Fine crackles of interstitial fibrosis or early congestive cardiac failure result from the sudden release of energy stored in the lung after delayed opening during inspiration of airways that had closed at the end of the previous expiration. These crackles rarely occur in expiration and are often localized over dependent areas of the lung, where gravitational stress predisposes the airways to collapse at low lung volumes. These crepitations do not disappear after coughing. Coarse crepitations occur in pulmonary edema and bronchiectasis when fluid is found in the airways, and are probably caused by rupture of fluid films or bubbles. Crackles occur both during inspiration and expiration.
Recently a mechanism whereby sound is generated by the motion of vortices in the human lung is described. This mechanism is believed to be responsible for most of the sound, which is generated both on inspiration and expiration in normal lungs.19 Mathematical expressions for the frequencies of sound generated, which depend only upon the axial flow velocity and diameters of the bronchi, are derived. This theory allows the location within the bronchial tree from which particular sounds emanate to be determined. Redistribution of pulmonary blood volume following transition from Earth gravity to the weightless state probably alters the caliber of certain airways and sound transmission properties of the lung. It is believed that these changes can be monitored effectively and noninvasively by spectral analysis of pulmonary sound.
More recently the computer technology and minidisk recorders have been used to analyze and characterize various breath sounds.20,21
MORPHOLOGICAL DIAGNOSIS
By the end of the clinical examination one will have a good idea of the three-step diagnosis outlined earlier. More clues will be available from the clinical history. Common pathological diagnoses made in various pulmonary diseases are outlined in Table 1.4. Sometimes one has to make a diagnosis of more than one pathological lesion like collapse with consolidation (Table 1.4); fibrocavitary lesion when features of fibrosis and cavity are present; and effusion with collapse when the mediastinal shift occurs on the same side instead of the usual shift to the other side, a finding observed in malignant pleural effusion due to bronchogenic carcinoma.
Sometimes one finds only few fine crepitations in a localized area without any other abnormal finding, which will not fit into a particular lesion. Therefore diagnosis like infiltration, fibrosis or pneumonitis is made according to the anatomical location of these findings and associated clinical history. Some lesions like chronic bronchitis, interstitial fibrosis, and bronchiectasis are self-explanatory and need not have one of those typical described lesions.
ANATOMICAL DIAGNOSIS
The right lung has three lobes and the left has two. The anatomical land mark for the major fissure runs between the 2nd thoracic spine in the back along the medial border of the scapula when abducted touching its inferior angle and joining the 6th costochondral junction in the front. This fissure divides the upper and middle lobes from the lower lobe in the right and the upper lobe and the lower lobe in the left side (it has no middle lobe). The right upper and middle lobes are separated by the minor fissure, which joins the major fissure in the anterior axillary line starting from the 4th costochondral junction. The anterior segments of the upper lobes on either side lie in the infraclavicular area, the apical segments in the supraclavicular area with some posterior extension and the posterior segments lie posteriorly above the major fissure (in the left, apico-posterior segment is one bronchopulmonary segment). The middle lobe in the right is represented around the mammary area.
The lingular segments of the left upper lobe are anterior structures and correspond to the area lateral to the precordium. The lower lobe segments lie mostly posteriorly with some lateral extensions. All the lobes are represented in the axilla. Thus, one can delineate the particular segment or lobe, which is affected by the particular pathological process.
ETIOLOGICAL DIAGNOSIS
Clinical history and physical examination will give reliable indications regarding the possible etiology of the underlying process such as an infective process (bacterial pneumonias, tuberculosis); and malignant diseases like bronchogenic carcinoma. Thus, in most cases a diagnostic formulation like ‘collapse of right upper lobe due to bronchogenic carcinoma’; ‘fibrocavitary lesion of the left upper lobe due to tuberculosis’; ‘right sided pleural effusion due to lymphoma’ and like wise, can be made out.
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Although most of the times this formulation is possible like a mathematical model, sometimes there may be difficulty. All the typical findings of a lesion may not be present. Therefore, one must make the best possible diagnosis by which all or most of the findings can be explained.9
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