An apparent increase in the anteroposterior (AP) diameter is also referred to as a barrel chest or pulmonary kyphosis. It occurs in pulmonary emphysema (or in patients with “senile kyphosis”). Interrater reliability for this sign is about 70% (Fletcher, 1952).

Actually, the AP diameter is not increased. In a study of 25 patients with emphysema, 22 patients with other diseases, and 16 normal subjects (Kilburn and Asmundsson, 1969), two physicians agreed that the 25 emphysema patients had an increased AP diameter. However, measurement of the actual inspiratory and expiratory AP diameters by chest film and by direct measurement with calipers revealed no significant differences between the three groups. Because the emphysema patients weighed about 30 pounds less than normal subjects, the “increased” AP diameter may be an illusory, albeit constant, field/image effect due to a decreased abdominal AP diameter.

Increased AP diameter does occur in acromegaly, along with kyphosis, as shown in Fig. 16-1.

Dyspneic and tachypneic persons with small-airway disease breathe in a pattern that is observably different from that exhibited by other dyspneic and tachypneic persons.

To acquaint yourself with the normal pattern of tachypneic breathing, exercise to the point of breathlessness, and then observe yourself in the mirror with your chest nude. Notice that your entire chest is moving and that you are taking deep breaths.

Patients with small-airway disease, in contrast, tend to “breathe off the top.” (The accessory muscles help them do this.) They take many small breaths from a position of relative inspiration but never seem to take very deep ones. If they do start to take deep breaths, they develop air trapping during expiration.

At end-expiration, the high transbronchial pressure can collapse the diseased terminal bronchioles, causing air trapping (and perhaps producing audible signs, see later in this chapter). These patients tend to exhale with pursed lips. In this way, they increase expiratory airway resistance and thus the pressure in the small collapsible airways, preventing collapse. Pursed lip breathing can lead to an increase in tidal volume, an increase in oxygen saturation, and a decrease in dyspnea. It reduces breathlessness by lengthening expiratory time and total time of the respiratory cycle (Bianchi et al., 2004). Because the airways are not at risk of collapse during inspiration, many patients who do purse their lips do it, quite unconsciously, only during expiration. This is a form of self-administered positive end-expiratory pressure (PEEP). Review Fig. 7-1 for the posture frequently assumed by patients with chronic obstructive lung disease.

Normally, the intercostal spaces bulge inward during inspiration and outward with expiration. This may be easily observed in a thin classmate.

An exaggeration of the inspiratory retraction occurs in patients with obstructive or restrictive lung disease because there is an imbalance between (a) the ability of the respiratory muscles to create a negative intrapleural pressure and (b) the impaired ability of the lungs to expand.

Focal exaggeration of inspiratory retraction indicates a regional imbalance in the two opposing forces discussed above. There might be a local obstruction with increased airway resistance, say in one of the bronchi. Or there might be a flail chest. In the latter, the affected ribs are separated from the rest of the chest, either by a fracture or by separation of the cartilages and thus, by their heightened inspiratory retraction, become a passive indicator of the underlying negative intrapleural pressure.

Focally exaggerated retraction of the cardiac interspaces, concordant with ventricular systole, is the Broadbent sign of constrictive pericarditis.

Unilateral or local loss of inspiratory retraction suggests an underlying consolidation, tension pneumothorax, or pleural effusion. In fact, even the small pleural effusion within the hydropneumothorax shown in Fig. 16-11 produced this sign.

Exaggerated expiratory bulging of the interspaces results from a mechanism similar to that of heightened inspiratory retraction. Diffuse expiratory bulging suggests that a positive intrapleural pressure is being effectively transmitted through the chest wall but that the lungs are not being emptied. This is a sign of increased expiratory airway resistance, either chronic (as in emphysema) or acute (as in asthma).

Focal expiratory bulging may be seen on the side of a tension pneumothorax or over the area of a flail chest. Constant focal bulging throughout all the phases of respiration can be caused by the accumulation of massive amounts of pleural fluid or very rarely by the underlying pulmonary consolidation.

Focal systolic bulging over the precordium is discussed in connection with the palpation of the point of maximum impulse (PMI) (Chapter 17). Focal systolic bulging anywhere else is a sign of an arterial aneurysm.

Normally, the abdominal wall moves passively outward during inspiration as the descending diaphragm squeezes the peritoneal contents down and out. Then, the abdominal wall retracts during expiration as the diaphragmatic piston returns to its resting position.

In weakness or paralysis of the diaphragm, most commonly owing to overwork in severe chronic obstructive lung disease, inspiration finds the helpless diaphragm being passively sucked upward as the intercostal muscles do the work of inspiration. Now the abdominal wall retracts during inspiration. This is called respiratory paradox (Macklem, 1982). The sophomore who observes this sign of diaphragmatic fatigue should immediately ask his resident to see the patient because the patient may be in need of mechanical ventilation.

False positives may be seen in vain persons wearing swimsuits who hope to be noticed. Such persons voluntarily contract the abdominal muscles during inspiration, as may be detected by palpation.

When the diaphragm is mildly impaired, it may work for a few inspirations and then fatigue for a few. When this happens, the abdominal wall may move out normally for a few inspirations and then paradoxically move inward for a few inspirations until the diaphragm is again rested. This sequence of events is called respiratory alternans (Macklem, 1982).

There are some marginal patients in whom respiratory paradox or alternans can be seen only in the perfectly erect position because when they lean forward (or rarely when they are supine) the increased intra-abdominal pressure can increase the dome of the flattened diaphragmatic leaves. This may improve efficiency to a degree that, in these marginal cases, allows the disappearance of the signs (Sharp, 1986).

The subcostal angle is the angle between the xiphoid process and the right or left costal margin, as shown in Fig. 16-2.

A second, less strict definition states that the subcostal angle is the angle between the right and left costal margins viewed from the patient’s feet. This more than doubles the size of the angle, allowing for easier appreciation of the changes. Also, the xiphoid process may be difficult to observe in obese patients. Finally, this second definition alleviates the problem of deciding which portion of the curved costal angle should be chosen for the chord or tangent that defines the angle; one simply takes any segment available and matches it to the facing side. However, several of the variations on the Hoover sign to be discussed below depend upon comparing the right and left subcostal angles, so this second definition will not be useful in that context.

With the patient sitting erect, visualize a line running from the symphysis mentis to the midpoint of the sternal notch. Ordinarily, the trachea will be on this line or slightly to the (patient’s) right of this line. Your findings can be verified by palpation (vide infra).

Note that tracheal deviations may be missed if they are sought with the patient lying in bed.

With lobar or segmental atelectasis of almost any etiology, the trachea is pulled toward the side of the atelectasis. On the other hand, it will be pulled to the side opposite that of a pneumothorax, especially during inspiration (Light, 1983). Tracheal deviation is commonly seen in upper-lobe collapse but rarely can be seen in collapse of the lingula or lower lobes (J. Arnett, personal communication, 1998).

Using the physical examination to determine the location of the trachea is one way of distinguishing between pleural effusion and consolidation with bronchial obstruction. In massive pleural effusion, the trachea is pushed away from the side that has the auscultatory findings; in massive consolidation with bronchial obstruction, the trachea may be pulled (by atelectasis) toward the side with the auscultatory findings. False negatives (which lack a tracheal shift) occur in uncomplicated pleural thickening, as well as in minor degrees of effusion, atelectasis, or consolidation without bronchial obstruction.

The trachea may be pushed away from a goiter. This can be a useful clue to the presence of a retrosternal goiter.

The trachea may be displaced anteriorly by an aberrant right subclavian artery.

A confusing picture may be found in situs inversus, in which the trachea may “normally” be slightly to the left.

Pleural thickening with parenchymal scarring may be distinguished from pleural effusion because in the former the trachea may be pulled toward the diseased side.

In some cases of severe unilateral pleural scarring or severe unilateral parenchymal fibrosis, the trachea appears to be midline but shifts toward the side of the lesion during a deep inspiration.

Tracheal deviation may also be seen with scoliosis.

Put your second and third fingers in the suprasternal notch and slide each as far laterally as possible to the heads of the clavicles. Is the distance from the lateral tracheal wall to the clavicular head the same on both sides? If so, the trachea is midline.

The various tracheal tug signs were discussed in Chapter 14.

It is said that low-frequency vibrations, such as those produced during the testing of vocal fremitus or by the cardiac impulse, are equivalent to a 128-Hz tuning fork and that the latter can be better felt by the “palmar base of the fingers” (the volar distal metacarpal heads) than by the tips of the fingers (DeGowin, 1965). This author’s observations, especially in men, do not confirm DeGowin statement. In the lone scientific study that compared the fingertips to the “palmar base” across a wide variety of frequencies in healthy young persons of both sexes, the fingertips were more sensitive (Lofvenberg and Johansson, 1984).

This is an important finding because the method offered above produces a wide spectrum of frequencies, and it is not clear which frequency is altered when tactile fremitus is “decreased.” In fact, 128 Hz would not be the best frequency to test for optimal function because that has been reported variously as 150 to 200 Hz (Goff et al., 1965) or 200 to 300 Hz (Lofvenberg and Johansson, 1984). The variability may be the result of studying groups with differing age and sex compositions because older persons have poorer vibratory sensation than younger persons (Goff et al., 1965; Roland and Nielsen, 1980), but the frequencies at which the threshold increases with age differ between men and women (Goff et al., 1965). The latter may explain why some report better vibratory discrimination for women (Roland and Nielsen, 1980), while others report better results for men (Goff et al., 1965).

There are situations in which the palmar base, the fingertips, or even the hypothenar surface of the hands seem to work better, and these are usually replicable between observers for any given
patient. The more important issue is to avoid missing a positive physical finding. I am unaware of anyone who has ever missed a lesion because of using the method given above.

Wiener and Nathanson (1976-1977) have difficulty comparing tactile fremitus from hands applied simultaneously to both sides of the chest. If you share this difficulty, you can use one hand applied sequentially in the same manner as one uses a stethoscope.

A common mistake is failure to attend to the pressure exerted by the hand when checking for tactile fremitus in fat people. If one does not compress the fat equally on both sides, one can get very peculiar results. This is most likely to happen when checking with only one hand at a time and alternating from side to side. Of course, this is not a problem with thin people, who were the major subjects of the great European physical diagnosticians of the late 19th and early 20th centuries, and that may explain why this caveat does not appear in the ancient tomes.

If you do not examine for tactile fremitus precisely in the manner described, you will probably do no better than the 25% agreement reported in a study of 24 British physicians (Spiteri et al., 1988).

Wiener and Nathanson (1976-1977) repeat the caveat of Norris and Landis (1938) that fremitus is normally increased in the right interscapular area; that is, it is comparatively decreased in the left interscapular area. The explanation is originally from the textbook of Norris and Landis (1,000 pages on the examination of the chest alone), which was cannibalized by Leopold (1952).

A beginner is advised to rate his findings of lateral disparity as definite or possible and to initially not use any of the latter in composing the differential diagnosis. Depending upon the number of chest examinations performed, the prevalence of pathology, and the quality of supervision, most students will require months to years to achieve a useful (i.e., better than radiographic) expertise.

A few general rules apply:

Place the third finger (pleximeter) of your left hand firmly against the surface to be percussed and then rap a pair of drum strokes on its distal phalanx using the tip of your right third finger as a mallet (the plexor). The first beat of the pair is strong; the second softer. The excursion of the plexor is up to 4 in. for the first stroke and less than 2 in. for the second stroke, but this varies widely with the percussor and the tissue that is being percussed. (This is really not a rule but only a general description of what beginners should try.) Some percussors strike only once (see Chapter 17).

Obviously, medical students with long fingernails are advised to clip them close, especially on the plexor hand.

Some people use the second finger and some the third finger as the pleximeter. Some strike over the fingertip and some over the distal interphalangeal joint. Some strike with their third finger, some with the second, and some with two or three fingers, and I have even seen descriptions of percussion by persons who use a tiny hammer as a plexor. This leads to the Student’s Rule of Percussion: There is no one correct way to percuss. Do whatever works best for you. It may help to remember a recurrent adage in percussion, attributed to Adolf Weil, that it is much easier to distinguish “something from nothing” than “more from less”; thus, if one percusses so lightly over a dull area that no note is produced, the same force of percussion will cause an audible tone to spring to life when a resonant area is encountered (McGee, 1995).

To facilitate each student in developing the percussion note that is best for him, I suggest finding someone who already knows how to percuss and have him teach you (and your partner) in the following manner:

Common errors include excessive use of force by the plexor finger, insufficient pressure on the pleximeter finger, delivering the blow through a motion at the elbow rather than the wrist, hitting the middle rather than the terminal phalanx of the pleximeter finger, and failure to move away promptly as does a piano hammer. One suggested method for overcoming these errors is to have students percuss directly on a tabletop and then indirectly through a foam sponge to simulate the skin and subcutaneous tissue. In this way, students rapidly learn the importance of correct technique, such as appropriate pressure by the pleximeter finger, in producing a clear sound (Benbassat and Meroz, 1988).

The question of whether the percussionist accomplishes his purpose by noting changes in sound or by feeling changes in vibratory quality was once debated enthusiastically. Probably both answers are correct at times. There are some situations in which one can continue to percuss accurately through the noise now so frequently encountered in teaching hospitals. But with other patients and other tissues, one is completely dependent upon the acoustic part of percussion and thus requires a silent room. Whatever the contribution of fingertip sonar to the percussionist’s ability to delineate underlying structures, it should be preserved in full because each of us needs all the help he can get. Accordingly, students who play steelstringed guitars or who for other reasons have fingertip calluses on their left hand are advised to percuss with their hands reversed. Thus, the noncalloused, sensitive right fingertip is the pleximeter struck by the left hand’s plexor.

Throughout this and other chapters, you will see the results of numerous studies attempting to validate (or debunk) various techniques of the physical examination. Results from one study to another may vary wildly. This could be because of an unmeasured, even unacknowledged, variable: the skill of the examiners. Often the methods section will recount the number of years spent in a given specialty or the fact that the examiners received some instruction in performing the technique before the study commenced. But had they practiced? Had they trained their hands and their ears, and had they correlated what they heard with the results of autopsy, surgery, radiographs, ultrasound, or other technologic studies?

Skill in surgery does not result from reading books or watching demonstrations and neither does skill in physical examination. One study showed that proficiency in cardiac auscultation correlated with the ability to play a musical instrument but not with a self-declared love for music nor with the habit of simply listening to music (Mangione and Nieman, 1997). The difference is in active, meticulous practice.

Do not percuss the chest with the patient positioned as shown in Fig. 16-3. For that matter, you should likewise never inspect, palpate, or auscult a patient so positioned, although the left lateral decubitus position is appropriate in situations described below.

This precept is based upon the fact that the dependent side may have false-positive signs produced by the acoustical damping and restricting properties of the bed or examining table that is touching the hemithorax. In difficult circumstances, one could conceivably examine the chest by rolling the patient from side to side, examining each hemithorax when it is superior. This would require a great deal of prior experience on the examiner’s part because he would have to “remember” what the other side sounded like if he were to use the information provided by nature’s control (the contralateral thorax). Moreover, Mazoon, who demonstrated the importance of cage resonance to the percussion note in autopsy studies, observed that any external pressure on the chest—from a pillow, a stretcher,
or an extra hand placed near the point of percussion—impeded chest wall motion and dampened the percussion note (McGee, 1995).

If the patient is unable to sit up because of stupor, muscular weakness, or some other inability to comply with the request, get someone else to hold him in a sitting position. Two persons standing by the sides of the bed, supporting the patient at the axillae, or sometimes only one person standing at the head of the bed holding the patient’s extended arms can accomplish this. The latter is especially useful in otherwise cooperative patients who are simply weak. Please note that this is also exactly what we should do when we need to have a portable chest film taken (vide infra). We should not accept the patient’s inability to sit or stand alone as an excuse for a poor chest film, nor should we accept it as an excuse for a poor physical examination.

A Note for the Senior Medical Student. When looking for internships, make rounds and observe the faculty at prospective hospitals. Do they examine only the anterior chest of a bed-bound patient, or do they examine the patient properly, with the house staff holding the patient up? This tells you what kind of data acquisition techniques you would learn in their programs.

Although the above method moves from above to below posteriorly, you might be just as well advised to learn to percuss from below to above—if you have not already developed a method—for reasons given below. However, whichever starting point you use, the important issue is to compare one side with the other. Note that in healthy, nonobese individuals, the percussion note may vary somewhat depending on the zone. In general, the posterior zones are generally less sonorous than the anterior ones because of the effects of muscle layer, scapulae, and lesser elasticity of the ribs. The axillary zone generally yields a more resonant sound, sometimes frankly tympanitic (Yernault and Bohadana, 1995).

In a pneumothorax, the alveolar tissue beneath the percussed finger is replaced by air that has leaked into the pleural space. Because there are no alveoli to act as tiny sound baffles, the percussion note over the pneumothorax is even more resonant than usual. It sounds more like the percussion note over the gastric air bubble than like that over a normal lung. However, because we are comparing right to left as we percuss the lung fields, the neophyte might assume the duller side to be the abnormal one. In the absence of changes to inspection or knowledge of the coin test, below, this assumption would lead one exactly in the wrong direction. The error should be immediately recognized when the breath sounds are found to be absent or decreased on the hyperresonant side. If large, a pneumothorax may result in a decreased chest excursion, and subcutaneous emphysema may be present.

Recently, it has been suggested that the best place to check for the hyperresonance of pneumothorax is over the midclavicle, with the patient sitting or standing erect (Orriols, 1987).

The Grocco triangle (Leopold, 1952) is a paravertebral triangle of dullness (relative, not absolute) whose right angle is formed by the spine and the normal diaphragm (Fig. 16-6). It is found contralateral to a pleural effusion but not to pleural thickening, and so may be used, if present, for the differentiation of the two processes. Note that it is a sign of relative dullness affecting the normal side.

The occurrence of the Grocco triangle is considered evidence to support the cage resonance theory. In a person without pleural
effusion, a Grocco triangle can be produced by external pressure over the opposite side of the chest, as from a hand or a bottle filled with water (McGee, 1995).

Other conditions that can produce a Grocco triangle (false positives) result from conditions that produce upward pressure upon the ipsilateral hemidiaphragm (ascites, gaseous distention, tumor, pregnancy, etc.), very large ipsilateral pericardial effusions, and massive contralateral pneumonia. If the patient has had a right pneumonectomy with an elevated right diaphragm (and liver), there may be a false positive on the left. This suggests that the mechanism has nothing to do with the “truly” normal lung but rather is an effect of acoustic muffling produced by the diseased side upon the “ normal” side of the Grocco triangle.

Any bilateral basal pulmonary process may confound the Grocco triangle, thus giving a false negative (Byfield, 1921).

For the Very Advanced Student. One can sometimes find a spot of egophony within Grocco triangle. Again, this happens in pleural effusion but not in pleural thickening.

In 1839, Skoda, the Czech physician (Sakula, 1981), described an area of hyperresonance above a pleural effusion (Fig. 16-7):

The mechanism for skodaic resonance is unknown.

Now, if the dullness over an area of pleural effusion were incorrectly attributed to the diaphragm, then the skodaic hyperresonance above it might be misinterpreted as normal and the resonant, but duller, contralateral side might incorrectly be thought to be the site of pathology.

The Ewart sign is dullness to percussion in the posterior lower left hemithorax, usually just under the tip of the scapula (Fig. 16-8). Because it results from a massive pericardial effusion distending the pericardial sac backwards and compressing the lung (the fluid-filled mass will not by itself produce the findings), it is obvious that all the physical signs of consolidation may he present.

The requirements for the Ewart sign include (a) a distensible pericardial sac that has not been previously scarred and (b) a massive chronic pericardial effusion that slowly stretches and distends it. Because patients now seldom go without medical intervention for sufficient time, the sign is found less frequently than in former years. Other percussive signs for pericardial effusion are discussed in Chapter 17.

It is not widely appreciated that massive pericardial effusion can also produce a right-sided Ewart sign, which should be called the Conner sign (Conner, 1926) (Chapter 17).

The space described by Ludwig Traube (also noted for his sounds, which are discussed in Chapter 17) is a semilunar space over the stomach air bubble. Internally, it is bounded medially by
the left lobe of the liver, laterally by the spleen, and superiorly by the lower border of the heart. On the surface, as shown in Fig. 16-9, it can be mapped by dropping perpendicular lines from the sixth rib at the costochondral junction and the ninth rib at the anterior axillary line to the costal margin. Over this space there should normally be, as described by Professor S. Jacoud in 1885, a “sharp tympanism with percussion, the absence of vocal vibrations by palpation and the absence of respiratory noise with auscultation” (Verghese et al., 1992). Findings described by Traube’s student Fraentzel include the following:

Jacoud added the caveats that reduction in the space may be the only sign of a subpulmonic effusion and that a reduction in the tympanism over the space could arise with pleural adhesions and not solely from pleural effusion. In the latter case, one should see retraction of the lower intercostal spaces with inspiration. It is said
that dullness over the Traube space is highly sensitive for effusions in an area where they can sometimes be missed by expert radiologists and that this has been confirmed on multiple occasions by thoracentesis.

The Traube space may be percussed with the patient either supine or sitting. For a patient with dullness in the left hemithorax, preservation of the Traube space suggests consolidation or atelectasis, while its obliteration suggests pleural effusion, except possibly in a patient with consolidation of the left anterior basal segment and the contiguous lingula.

Dullness in the Traube space could also be a sign of splenic enlargement (see Chapter 20), though this application was never described by Traube.

For the Attending. Findings such as this can cause “slack-jawed expressions of wonder on the faces of students and house staff when bedside diagnosis correlates with roentgenologic diagnosis—as if an insidious and deeply rooted distrust of the hands-on examination is being shaken. It is ironic that the ready availability of diagnostic technology has not, it seems, enhanced bedside skills but instead has encouraged their atrophy” (Verghese et al., 1992).

Note that this is not an exact technique. One is more concerned with the relative positions of the right and left hemidiaphragms in expiration and deep inspiration.

When you become proficient, you will shorten this technique to just one pass on each side.

Actually, the hemidiaphragms cannot be percussed in their three-dimensional surface, nor do the body-wall insertions of the hemidiaphragms change during percussion. Rather, we determine the amounts of aerated lung near the body surface allowed by the changing shape of the hemidiaphragms and call these the “movement” of the “diaphragm” or of the “hemidiaphragms.”

Normally, the percussed resting positions of the two hemidiaphragms are equally high, or the right hemidiaphragm is a little higher than the left. Usually, both of them appear to move the same distance. Evidence for bilateral movement may be lost in extremely fat persons, persons who normally breathe from a position of relative inspiration (the emphysematous), or individuals with severe restrictive disease who are unable to take a deep breath. It is possible in normals for the left hemidiaphragm to move a bit more than the right, but it is still an indication to search for disease on the right.

If the resting position of the left hemidiaphragm is higher, this is definitely abnormal. There are several possible explanations: (a) The left hemidiaphragm may be paralyzed. In this case, the right hemidiaphragm will move down with inspiration, but the left will move paradoxically: up with inspiration, down with expiration. (b) There may be a left lower-lobe lesion, causing an area of dullness that is indistinguishable from the left hemidiaphragm. (c) Rarely, a giant pericardial effusion will give a false-positive sign for an elevated left hemidiaphragm (the Ewart sign, discussed earlier in this chapter). (d) There may be a left upper quadrant abdominal mass, such as an enlarged kidney or spleen. In the last three conditions (b to d), the left hemidiaphragm, besides being higher, may seem to move only slightly, if at all, with respiration. (e) Very rarely, the patient may have situs inversus abdominalis.

If the right diaphragm is higher than the left, one might dismiss it as a normal variant. But all of the phenomena that can cause the left hemidiaphragm to be higher than the right and that can impede the respiratory excursions can also afflict the right side, mutatis mutandis. Because the right hemidiaphragm in normal persons is sometimes perceived to move less than the left, one cannot be dogmatic about the presence of pathology on the right side unless there is clear evidence of paralysis or of paradoxical motion. Diminished diaphragmatic excursion correlated with chronic obstructive pulmonary disease (COPD) in one study but not in another. In the positive study, a percussed excursion of less than 2 cm detected COPD with a specificity of 0.98 but with a sensitivity of only 0.12 (Badgett et al., 1993).

Wiener and Nathanson (1976-1977) state that the hemidiaphragms normally move 5 to 7 cm by percussion and that the right hemidiaphragm is normally percussed 1 or 2 cm above the left. Most will usually agree with these figures, but percussion yields sufficient interobserver variability, especially among young examiners, that one should not diagnose an abnormality based solely upon the violation of either of these putative ranges of normality.

Macklem has pointed out that a better way to detect failure of descent of the hemidiaphragm on one side may be by palpation of the abdomen. The side that fails to descend will generate noticeably less abdominal pressure on that side (Macklem, 1986).

The mediastinum will also shift away from the side of poor diaphragmatic descent, but most do not percuss the mediastinum in both full inspiration and expiration.

Two observers, one of whom was clearly the clinical superior of the other, determined diaphragmatic excursion by percussion in
29 patients (Williams et al., 1981). The authors were disappointed that they only agreed with each other (within 2 cm) about 60% of the time.

There are, of course, times when percussion of the diaphragm is, for one reason or another, as indeterminate as percussion of the heart size and contour may be. But there are other times when a disparity between the two sides is clearly detectable.

I agree that some persons are unable to percuss out diaphragmatic descent—my Aunt Minnie, for example.

Before reading on, answer the study question in the legend to Fig. 16-4.

Bailey (Clain, 1973) could find four zones of percussion in a patient with a subphrenic abscess. The diaphragm lies between zones 1 and 3. Zone 1 is normal lung, zone 2 is compression atelectasis, zone 3 is gas in the abscess, and zone 4 is the normal dullness of the liver.

An internist would find this pattern of percussion more commonly in a right lower-lobe pulmonary consolidation that afflicts a superior posterior portion of the right lower lobe (viz., zone 1 is again the normal lung, zone 2 is atelectatic or consolidated lung, zone 3 is the most inferior portion of the right lower lobe, and zone 4 is again liver dullness). Here, the diaphragm is located between zones 3 and 4. To distinguish the two situations, simply listen over zone 3. If you hear breath sounds, you know that you are listening to the lung, that the diaphragm is between zones 3 and 4, and that the dullness to percussion in zone 2 must represent intrapulmonary consolidation not afflicting the most basal segments of the right lower lobe. If, on the other hand, there are no breath sounds in the resonant zone 3, you could assume that you are listening over the gas in a very large subphrenic abscess. (If the gas were in a pulmonary abscess, you might hear amphoric breathing, discussed later in this chapter).

Note that Bailey could never have made this distinction because the apparatus used for diagnostic purposes in his book (his Fig. 1) does not include a stethoscope, nor is the word “stethoscope” to be found in the index. (Conversely, the methods outlined in the present text would be all but useless for attempting to diagnose pericardial calcification. This teaches us that our diagnostic experience is totally dependent upon the tools we use to search for disease.)