1 What are the main components of the chest exam?

They are the same as for any other section of the exam: inspection, palpation, percussion, auscultation, and … contemplation. This last (but not least) component was added by William Osler, as the necessary pondering of information garnered through the four preceding stages. Pondering was so important for Sir William that several portraits actually depict him at the bedside, deeply engrossed in his own contemplative thoughts. Yet, with the fading of bedside rounds, contemplation took a hit, becoming the latest casualty in the never-ending feud between science and art for the soul of medicine.

2 What is the usual sequence in a typical pulmonary exam?

The patient usually remains seated, with the physician moving from front to back and sides. Initial assessment includes an evaluation of effort, rate, and depth of respiration. It also should identify any wheeze, or grunt, or noisy sound that might be audible without the need of a stethoscope. Sequential inspection of the anterior, posterior, and lateral chest should then be carried out. Finally, palpation, percussion, and auscultation complete the exam. The examination should be thorough and go from the chest surface toward the inner structures (Fig. 13-1).

Figure 13-1 Algorithm for the nonauscultatory pulmonary examination.

3 What kind of information can be gathered through inspection?

In addition to gross abnormalities of body habitus (such as the Pickwickian type of obesity-hypoventilation or sleep apnea), an astute examiner also should look for seven important areas of anomaly:

4 What are the most common abnormalities of respiration?

Mostly the ones related to the vital signs of the respiratory pump, such as pattern of breathing and its three main components: (1) rate, (2) depth, and (3) rhythm. Each of them may be abnormal, and all may be evaluated by simply observing the patient during the interview. In addition, grunting, nasal flaring, and pursed-lip respiration also can be detected through bedside observation (see later).

5 What are the abnormalities of posture?

These, too, can be detected by simple observation, even before the patient undresses. They are mostly related to compensatory postures, designed to improve the efficiency of the respiratory “pump.” Patients with chronic obstructive pulmonary disease (COPD), for example, usually sit up and lean forward, so that they can better tense the accessory respiratory muscles and improve their contractility. Patients may lean so much forward to eventually have to prop themselves up by their resting elbows against the thighs. With time, the protracted pressure on the thighs leads to hyperpigmented calluses immediately above the knees (Dahl’s sign).

6 What are the main abnormalities in the use of respiratory muscles?

In addition to recruitment of accessory muscles of respiration, the main abnormality is an asynchronous contraction of the diaphragm and intercostals (paradoxical respiration), an important sign of impending respiratory failure.

7 What about asymmetry in thoracic expansion?

This, too, can be detected by simple inspection, even though it is usually best evaluated by palpation.

8 What abnormalities of the chest cage can be detected by inspection?

Abnormalities of the spine, ribs, and sternum. All may adversely affect lung mechanics and thus lead to compensatory postures.

9 And what about abnormalities of the chest surface?

They are pallor or cyanosis, hyperpigmentation or hypopigmentation, expiratory bulges, collateral circulations, dermatomic lesions, and chest wall fistulas. All are detectable by astute observation.

10 What about assessment of extremities and neck veins?

Although often carried out separately, examination of neck veins and extremities is an important aspect of respiratory evaluation. Finding clubbing, for example, or asterixis may provide valuable information toward the recognition of an underlying respiratory disease. The same can be said for the detection of either nicotine stains (usually on fingers) or a smoker’s face (deep and premature wrinkles coupled with skin coarsening), both indications of unrepentant smoking even before a social history is obtained. Finally, distended neck veins in patients with either cor pulmonale or pulmonary embolism also can be a very important diagnostic sign.

(1) Abnormalities of Respiration

12 Can tachypnea be considered normal?

Probably not. Still, a respiratory rate >20 breaths/minute is often seen in elderly nursing home residents with chronic medical conditions but no active disease.

13 What is the clinical significance of true tachypnea?

It usually indicates moderate to severe cardiorespiratory disease, requiring a compensatory increase in the work of breathing. In hospitalized patients, it carries a bad prognosis. In fact, on internal medicine wards, it predicts cardiorespiratory arrest. It also argues in favor of pneumonia, both in the inpatient and outpatient settings. In hospitalized pneumonia patients, it can even predict death, thus providing a far more accurate prognostic indicator than either tachycardia or abnormal blood pressure. It also predicts failure to wean from mechanical ventilation.

14 Can absence of tachypnea be helpful?

Yes, because tachypnea is so common in chest diseases that its presence adds relatively little, whereas its absence challenges a cardiac or respiratory diagnosis. For example, tachypnea is so frequent in pulmonary emboli (92% of patients) that a normal respiratory rate argues strongly against the diagnosis. The same can be said for tamponade, where tachypnea is a must. Conversely, in an acute abdomen, tachypnea directs attention to a supradiaphragmatic rather than subdiaphragmatic process.

15 Does tachypnea predict hypoxemia?

Not necessarily. In fact, some patients might actually be hypoxic as a result of hypoventilation (and therefore of bradypnea). Others might use instead tachypnea to fully compensate for hypoxemia. Hence, the need for monitoring not only the respiratory rate, but also oxygen saturation.

16 What is the clinical significance of bradypnea?

It should prompt consideration of hypothyroidism, but it also may suggest a central nervous system disease, or, as indicated before, the use of narcotics and sedatives.

17 What is apnea?

It is the absence of respiration for at least 20 seconds while awake or 30 seconds while asleep. It is often seen in patients with either neuromuscular dysfunction (central apnea) or airway obstruction induced by rapid eye movement (REM) sleep (obstructive sleep apnea). Note that apnea also remains the final event of all respiratory failures, whether due to pulmonary or neuromuscular disease.

Abnormalities in the Depth of Respiration

18 What are the main abnormalities in the depth of respiration?

Hyperpnea and hypopnea (Fig. 13-2).

Figure 13-2 Patterns of respiration. The horizontal axis indicates the relative rates of these patterns. The vertical swings of the lines indicate the relative depth of inspiration.

(Adapted from Seidel HM, Ball JW, Dains JE, Benedict GW: Mosby’s Guide to Physical Examination, 3rd ed. St. Louis, Mosby, 1995.)

19 What is hyperpnea?

It is an increase in tidal volume, usually accompanied (but not necessarily) by an increase in rate. In other words, hyperpnea is a rapid and deep respiration. The classic form was first described by Kussmaul in patients with diabetic ketoacidosis, who attempt to compensate by hyperventilating. This compensation also can be observed in any of the other anion gap metabolic acidoses, which can be recalled with the mnemonic make up a list: methanol poisoning, aspirin intoxication, ketoacidosis, ethylene glycol ingestion, uremia, paraldehyde administration, and lactic acidosis.

20 Is there a difference between hyperpnea and the hyperventilation of cardiorespiratory disease?

Yes. In cardiorespiratory disease, vital capacity is typically compromised, and thus breaths are shallow, with the increase in ventilation due primarily to a faster rate. In contrast, true hyperpnea relies more on increased tidal volume. Since this does not rebreathe dead space as much, it is a better CO₂ controller. Hence, hyperpnea rather than tachypnea is the compensation of choice in metabolic acidosis.

21 Who was Kussmaul?

Adolf Kussmaul (1822–1902) was a graduate of Heidelberg and Würzburg (where he studied under Virchow) and a part-time German Army surgeon. He was the first to describe periarteritis nodosa and progressive bulbar paralysis. He also was the first to attempt gastroesophagoscopy, pleural tapping, and peritoneal lavage. His name is linked to the respiration of patients with metabolic acidosis, the clinical description of pericarditis, pulsus paradoxus, aphasia, and, of course, Kussmaul’s sign, the inspiratory increase in jugular venous pressure (and distention) seen in patients with obstruction to right-sided venous return (see Chapter 10, questions 115–118). A meticulous and precise man famous for complaining that none of his colleagues could write good German, Kussmaul contributed satirical poems to a weekly magazine under the pseudonym of Gottlieb Biedermeier, an imaginary and unsophisticated poet who eventually came to symbolize the values and tastes of the early 19th-century German bourgeois: reliable, hard-working, but boringly unimaginative (like in the Biedermeier style of furniture. “Bieder” is German for “everyday, plain” while “Meier,” or Meyer, is a common German last name).

22 What is hypopnea?

It is shallow respiration, usually indicative of impending respiratory failure or obesity-hypoventilation (Pickwickian syndrome). In this regard, hypopnea is often associated with periods of apnea (see question 17).

Abnormalities in Rhythm and Pattern of Respiration

24 What is Cheyne-Stokes respiration?

It is a form of periodic breathing (i.e., a regularly irregular pattern consisting of a series of cycles). Each “cycle” has a constant respiratory rate but variable depth, insofar as it progressively increases in amplitude (crescendo), eventually culminating in a peak followed by a decrescendo period. This fades into complete apnea, from which another cycle restarts. The crescendo-decrescendo phase lasts approximately 30 seconds, whereas the apneic period is usually just a little shorter.

25 What is the physiologic repercussion of Cheyne-Stokes?

Mostly a swing in cerebral blood flow, caused by alternating hyperpnea (higher cerebral flow) and hypopnea (lower cerebral flow). These are probably responsible for some of the mental status changes described in these patients, such as alertness, agitation, and increased muscle tone during hyperpnea, followed by sleepiness, motionlessness, and decreased tone during apnea.

26 What is the clinical significance of Cheyne-Stokes?

27 What are the therapeutic implications of Cheyne-Stokes?

Given its major swings in ventilation (and O₂ blood levels), patients with Cheyne-Stokes respiration may require administration of supplemental oxygen and, overall, have a worse prognosis.

28 Who were Cheyne and Stokes?

John Cheyne (1777–1836) was a Scot and himself the son of a surgeon, often helping his father to care for patients by bleeding and dressing them. After graduating at age 18 from the University of Edinburgh, he served in the army for 4 years. During this time, he took part in the battle of Vinegar Hill, which broke Irish resistance to British rule. In 1809, he went to Dublin, where he was eventually appointed Physician-in-General for Ireland, becoming the founder of modern Irish medicine.

William Stokes (1804–1878) was instead a bona-fide Irishman and the son of the anatomy professor who had succeeded John Cheyne at the College of Surgeons School in Ireland. Although lacking in formal education (his father wanted to protect him from a society that did not abide by the scriptures), Stokes eventually went to Edinburgh, where he received his doctor of medicine in 1825. In Scotland, he learned of Laënnec and his recent invention, the “cylinder.” He soon became so enamored of this little tool that he even wrote an introductory book about it, the first of its kind in the English language. In fact, Stokes was such a vocal advocate for the use of stethoscopy that he provoked quite a few reactions (and even some sarcasm) among his colleagues. Still, he was a well-liked physician, who worked among the poor during the Dublin typhus epidemic in 1826 (he even contracted the disease but survived) and then again during the subsequent cholera epidemic. His name is linked not only to the eponymous pattern of respiration but also to Stokes-Adams syncope, which the Irish surgeon Robert Adams had described in 1827 and which Stokes included in his 1854 book, Diseases of the Heart and Aorta. Of course, the Italian Morgagni had preceded them both by describing the condition almost 100 years before (see Chapter 11, question 14).

29 What other abnormalities in rhythm are worthy of recognition? What is their significance?

30 What is a grunting respiration?

It is another abnormal respiratory pattern. A typical grunting respiration is the râle de la mort, a pre-terminal gurgling-and-grunting sound produced by patients too ill to clear secretions. The expression translates as “death rattle” (râle is rattle in French), and in the olden days, it used to be a sign of severe pneumonia with impending respiratory muscle fatigue and death. The râle de la mort also is the main cause of Laënnec’s botched nomenclature, insofar as the inventor of the stethoscope became so sensitive to the emotional overtones of the term râle to eventually prefer at the bedside its Latin equivalent rhonchus. This triggered a tremendous (and ongoing) confusion in lung sound terminology.

31 What is the clinical significance of a grunting respiration?

Very much the same as in Laënnec’s days. It can still be heard in adults with respiratory muscle fatigue (and impending arrest), but nowadays it is much more frequent in children, where it usually presents as a short and low-pitched noise produced by forced expiration against a closed glottis. The “grunt” is due to the sudden opening of the glottis and the loud rush of air from the larynx. Its physiology (and significance) is akin to pursed-lip respiration (see below, questions 32 and 33), insofar as it leads to an increase in expiratory airway pressure, which then acts as a mechanical splint against alveolar collapse, increasing tidal volume and oxygenation while decreasing respiratory rate and CO₂. An increased intra-alveolar pressure also has a positive effect against transudation of fluid in patients with pulmonary edema, and thus it is often observed during acute episodes of left ventricular failure.

32 What is pursed-lip respiration?

Another respiratory pattern, typically seen in obstructive lung disease—usually emphysema (Fig. 13-3). Given the alveolar hyperinflation (and reduced lung elasticity) of COPD, patients are at risk for expiratory airway closure and air-trapping. Hence, they resort to pursed lip exhalation, as if they were inflating a balloon. This increases intra-airway pressure, thus inducing auto-PEEP (positive end-expiratory pressure). It is often accompanied by an expiratory wheeze or grunt.

Figure 13-3 Demonstration of pursed-lip breathing in patients with COPD and its effects. The weakened bronchial airways are kept open by the effects of positive pressure created by pursed lips during expiration.

(From Hillegass EA, Sadowsky HS [eds]: Essentials of Cardiopulmonary Physical Therapy. Philadelphia, WB Saunders, 1994.)

33 What is the physiologic impact of pursed-lip respiration?

It increases arterial O₂ while decreasing CO₂. It does so by behaving as an E-PAP in a Bi-PAP machine (i.e., by providing an expiratory positive airway pressure). It also slows respiratory rate (by as much as 40%), improves tidal volume, and decreases dyspnea. The mechanism for the latter is unclear, although it probably involves an effect on interstitial J-receptors as well as an overall reduction in the work of breathing.

34 What is nasal flaring?

It is the outward inspiratory motion of the nostrils—a valuable sign of respiratory distress. Often associated with the use of accessory muscles.

(2) Abnormalities of Posture

36 What is orthopnea?

It is a dyspnea that is aggravated by lying flat. Conversely, it is relieved by sitting upright. It comes from the Greek orthos (upright) and pneo (breathing)—(i.e., upright respiration).

37 What is the clinical and physiologic significance of orthopnea?

Usually indicates congestive heart failure, where it can help identify patients with low ejection fraction. Conventional wisdom has traditionally interpreted orthopnea as a “poor man’s” phlebotomy, pooling blood in the dependent areas of the body and thereby decreasing venous return and ventricular preload. Yet, in patients with congestive heart failure, orthopnea and pulmonary capillary wedge pressure correlate very little. Still, the need for orthopnea is often relieved whenever left ventricular failure degenerates into bi-ventricular failure, suggesting that failure of the right ventricle may indeed provide a useful “unloading” to left ventricular filling and pulmonary congestion.

38 Can orthopnea also occur in patients with lung disease?

Yes. Although more common in heart disease (in as many as 95% of cases), orthopnea also may be observed in lung disease, since sitting upright improves both vital capacity and lung compliance. Hence, orthopnea can occur in many pulmonary conditions, such as pneumonia, bilateral diaphragmatic paralysis, and pleural effusion. It also can occur in bilateral apical lung diseases, usually bullous. Whenever these patients sit up, they increase perfusion to the lower lung fields (as a result of gravity). Since these areas also are the best ventilated (because of bilateral apical disease), orthopnea improves ventilation/perfusion matching and gas exchange and thus relieves dyspnea.

39 And what about patients with COPD?

In COPD (which often presents with apical bullae), an upright position improves not only gas exchange but also lung mechanics (because of the increased stretch of accessory respiratory muscles). Hence, COPD patients often tend to prop themselves up, so that they can better use their respiratory muscles. They do so by clasping the side of the bed or pushing with the elbows over the thighs (see question 5, Dahl’s sign).

40 What about asthma?

Orthopnea also is an important sign of asthma, especially severe asthma. In fact, when present at the time of initial emergency evaluation, it is a good predictor of poor outcome. Patients who cannot lie flat have a worse pulmonary function and a greater need for admission. The same is true for diaphoresis. Both findings were reported by Brenner in acute asthmatics and represent the scientific validation of the time-honored dictum that patients who “do not look good” (because they are sweaty and in an obligatory upright position) usually do poorly.

41 So, is orthopnea a cardiac or a pulmonary sign?

It is both. Because of all the above reasons, orthopnea should not be interpreted as a sign of a cardiac rather than respiratory etiology. The contrary is actually the case. Yet, absence of orthopnea in pulmonary patients does argue against concomitant presence of left ventricular failure.

42 Can orthopnea be encountered in patients with neither cardiac nor pulmonary disease?

Yes. For instance, it can be seen in patients with massive ascites, obesity, or bilateral phrenic nerve paralysis. In both cases, an upright position helps relieve the intra-abdominal pressure on the lungs.

43 What is PND?

It is a very common and dramatic presentation, characterized by a nocturnal spell (paroxysm) of acute dyspnea (air hunger). After 1–2 hours of sleep, the patient suddenly awakens, sits upright, lowers the legs down the side of the bed, opens the window to catch some fresh air, and after a few minutes feels better enough to go back to sleep.

44 What is the mechanism of relief in PND?

It is the upright posture, of course, and not the fresh air (although cold air blown into the face of patients has been shown to give a refreshing feeling in both cardiac and pulmonary diseases). The peripheral blood-pooling caused by sitting upright effectively decreases venous return, thereby reducing pulmonary capillary pressure and lung congestion. PND is, therefore, a frequent sign of left ventricular failure.

45 Can PND be seen in pulmonary patients, too?

Yes. Like orthopnea, it can be seen in bullous and bilateral apical disease. Both basilar perfusion and lung mechanics are improved when the patient sits upright and leans forward.

46 What is platypnea?

From the Greek platus (flat) and pneo (respiration), platypnea is an obligatory supine respiration. In other words, patients with platypnea breathe better when they lie flat. Hence, it is the opposite of orthopnea: it is a dyspnea in the erect position, promptly relieved by recumbency. Platypnea is often associated with orthodeoxia, which is a hemoglobin oxygen desaturation upon sitting upright.

47 What is the clinical significance of platypnea?

Unlike orthopnea, platypnea is usually due to a right-to-left shunt, which can be either intracardiac or intrapulmonary. In intrapulmonary shunts, platypnea requires a bibasilar process (and not biapical, like orthopnea). In this case, an upright posture increases perfusion to the lower lobes, worsens ventilation/perfusion (V/Q) matching, and leads to oxygen desaturation and dyspnea. Conversely, a supine position improves V/Q matching and relieves dyspnea. Given its physiology, platypnea occurs in:

48 What is trepopnea?

From the Greek trepo (twisted) and pneo (breathing), this is a “twisted respiration” characterized by the patient’s inability to lie supine (or prone), and instead by preference for the lateral decubitus position. Trepopnea is often referred to as “down with the good lung,” meaning that in cases of unilateral lung disease, the patient can breathe better when placed on a side, typically with the good lung down.

49 What is the physiology behind trepopnea?

It is an increased perfusion to the dependent lung, which happens to be the good one, thus causing better (V/Q) matching, better oxygenation, and more comfortable respiration.

50 What are some of the disease processes associated with trepopnea?

The classic one is a unilateral lung collapse, from an endobronchial obstructing lesion or a massive effusion. In both situations, the patient feels better (and has improved oxygenation) whenever the good lung is “dependent.” A similar mechanism also can explain the preferential right lateral decubitus position of patients with congestive heart failure from dilated cardiomyopathy (since this relieves the pressure applied on the left lung by the enlarged heart), or the preferential lateral decubitus position of patients with a mediastinal or endobronchial tumor that compresses the airways only in a particular position.

51 Are there any contraindications to lying with the “good” lung down?

Any unilateral lung disease due to “spillable” material, like pneumonia (intra-alveolar pus) or hemorrhage (intra-alveolar blood). In this case, intrabronchial spread into the dependent good lung would only make things worse. Hence, patients with “spillable” unilateral disease should always lie with the bad lung down, since protecting the good lung is more important than improving oxygenation. Finally, lying with the good lung down is physiologically detrimental in small children with unilateral lung disease.

(3) Abnormalities in the Use of Respiratory Muscles

53 What is abdominal paradox?

It is a sign of diaphragmatic fatigue. During normal respiration, the abdominal and thoracic wall are synchronized, both expanding in inspiration and contracting in exhalation (even though chest expansion is usually greater in the upright position, whereas abdominal expansion is usually greater in the supine position). In some conditions, however, the chest and abdomen become asynchronous, with the chest expanding in inspiration while the abdomen is instead being pulled in and vice versa. This “rocking motion” (labeled abdominal paradox, paradoxical respiratory breathing, or respiratory paradox) usually indicates bilateral diaphragmatic weakness or paralysis, causing the diaphragm to behave as a passive membrane, sucked up into the chest during inspiration and pushed down into the abdomen during exhalation.

54 What is the best way to detect abdominal paradox?

Bimanual palpation. Lay one hand over the patient’s chest and one over the abdomen—then look for rocking motion. Note, however, that “paradox” also can be detected by simple inspection.

55 Are patients with abdominal paradox orthopneic?

Yes. Since in a supine position the abdominal content applies greater pressure on the diaphragm, patients with abdominal paradox try to compensate by assuming an upright posture.

56 How clinically valuable is this maneuver in predicting respiratory failure?

Quite valuable. Abdominal paradox has high sensitivity (95%) and good specificity (71%). In fact, in impending respiratory failure, it usually precedes deterioration of arterial blood gases.

57 What is asynchronous breathing?

It is a special form of abdominal paradox, seen in patients with chronic obstructive lung disease. In this case, the inward movement of the abdominal wall in early exhalation is almost immediately followed by an outward movement. This particular form of expiratory “rocking” reflects worse pulmonary function and prognosis, predicting respiratory failure, requirement for mechanical ventilation, and death.

58 What is respiratory alternans?

Another sign of respiratory muscle weakness and impending failure. It may occur in place of, or in combination with, abdominal paradox. Patients with respiratory alternans exhibit alternate use of either the diaphragm or intercostals, with the chest and abdomen first “rocking” one way, and then the other way. Occasionally, patients may cycle from respiratory alternans to abdominal paradox and vice versa.

59 How is respiration in patients with peritonitis?

Limited. In peritonitis, the abdominal wall can become quite still during respiration. This limitation in movement is diffuse in generalized peritonitis and localized in focal involvement. In diverticulitis, for example, the motionless area is the left lower quadrant; in appendicitis it is the right lower quadrant.

(4) Asymmetry in Thoracic Expansion

61 What is the best way to identify a thoracic asymmetry by inspection alone?

Deep inspiration, since these lags are typically undetectable during quiet respiration. Hence, ask the patient to take a full deep breath and then look for a local lagging in chest expansion.

(5) Abnormalities of the Chest Cage

63 What are the main chest cage abnormalities?

It depends on whether they involve the spine, sternum, or ribs. Often, more than one component is affected.

Abnormalities of the Spinal Column

65 What abnormalities may be seen on the sagittal plane?

These are an increase in spinal convexity (lordosis) or concavity (kyphosis)—often coexisting.

66 What abnormalities may be seen on the frontal plane?

These are lateral spinal curvatures, also called scoliosis (from the Greek word for crookedness). Depending on etiology, a scoliosis may have one curvature, or two curvatures (a primary and a secondary, with the latter providing a compensatory function). Scoliosis also may be fixed (because of muscle and/or bone deformity) or mobile (because of unequal muscle contraction) (see Fig. 13-4).

Figure 13-4 Deformity of vertebrae and rib cage in scoliosis illustrating the lateral curvature and rotation of vertebrae.

(From Schidlow DV, Smith DS: A Practical Guide to Pediatric Respiratory Diseases. Philadelphia, Hanley & Belfus, 1994.)

67 What is kyphoscoliosis?

A typical example of a mixed abnormality: scoliosis plus kyphosis. This is a very common problem, especially in our aging and increasingly osteoporotic population. In fact, the incidence of spinal deformities in the United States is now 1/1000 for mild cases and 1/10,000 for more severe forms.

68 Is physical exam the best way to assess kyphoscoliosis?

No. Chest examination allows detection of the abnormality, but is of little value in quantifying its degree. To do so, you must rely on chest radiographs, and on the determination of the Cobb angle of scoliosis (Fig. 13-5). This can be calculated by drawing two lines parallel to (1) the upper border of the highest and (2) the lower border of the lowest vertebral bodies of the primary curvature, as seen on a spine anteroposterior (AP) film. The angle is then measured at the intersection points of two additional lines, drawn perpendicular to the original lines. As a rule of thumb, a Cobb’s angle of 10 is considered the minimum angulation for a definition of scoliosis. Conversely, a Cobb’s angle >100 degrees represents a severe deformity, one associated with higher risk for pulmonary hypertension and respiratory failure.

Figure 13-5 How to draw and measure the Cobb angle.

(From Staheli LT: Pediatric Orthopedic Secrets. Philadelphia, Hanley & Belfus, 1998.)

69 What are the most common causes of kyphoscoliosis?

Idiopathic

Neuromuscular

Muscular dystrophy

Poliomyelitis

Cerebral palsy

Friedreich ataxia

Vertebral

Osteoporosis

Osteomalacia

Vitamin D-resistant rickets

Tuberous spondylitis

Neurofibromatosis

Disorders of connective tissue

Marfan syndrome

Ehlers-Danlos syndrome

Morquio syndrome

Thoracic cage abnormality

Thoracoplasty

Empyema

70 What is a gibbus?

It is the Latin word for hump (or hunch), the lay term for a sharply angulated spinal deformity with the apex pointing posteriorly. In medical terminology, a hunchback (or humpback) is a severely kyphotic patient.

71 What are the consequences of these spinal column abnormalities?

Other than esthetic, the consequences are primarily respiratory—and often quite dramatic, too. In fact, if severe enough, any of these abnormalities can so compromise respiratory mechanics as to cause localized hypoventilation. In turn, the resulting V/Q mismatch leads to localized hypoxemia, pulmonary vasoconstriction, pulmonary hypertension, and eventually right-sided heart failure. Given its prevalence in an aging population, severe kyphoscoliosis is a common cause of cor pulmonale. In fact, chest cage abnormalities are among the few conditions that may result in severe right-sided failure despite lungs that are entirely normal (the others being obesity-hypoventilation and sleep apnea).

Abnormalities of the Sternum

73 What is a funnel chest?

It is a deep sternal depression, characterized by backward displacement of the lower half (or two thirds) of the sternum, often more visible after a deep inspiration. The alternative term, pectus excavatum (which is Latin for “hollow chest”), reflects the defining characteristic of this lesion (Fig. 13-6). In fact, even the upper part of the abdomen is often depressed, making it resemble a “potbelly.” Note that a funnel chest may compress not only the lungs (and thus distort pulmonary mechanics), but also the ventricles—especially the right one because the sternal deformity is often asymmetric, displacing the heart toward the left as well as compressing the right chambers.

Figure 13-6 Pectus excavatum.

(From James EC, Corry RJ, Perry JF: Principles of Basic Surgical Practice. Philadelphia, Hanley & Belfus, 1987.)

74 How common is pectus excavatum?

Quite common, present in 1 of every 300–400 births. Although occasionally associated with specific diseases (such as rickets, acromegaly, or Marfan syndrome), a funnel chest is much more likely to be sporadic or familial and thus inherited. Other musculoskeletal problems are often present, especially scoliosis, seen in approximately 20% of these patients.

75 When does a funnel chest become recognized?

Usually after birth, even though it often progresses with age, eventually peaking after puberty and the growth spurt. Spontaneous improvement is rare because cartilages and ligaments are fixed.

76 What are the symptoms of a funnel chest?

In addition to its cosmetic and psychologic implications (such as shyness and excessive reluctance toward activities where the chest is being exposed—like swimming), most symptoms tend to occur only after significant physical effort, such as the one required by athletic competition. Hence, patients often remain asymptomatic until early adulthood. Mild defects are usually associated with only decreased endurance, or easy fatigability. More severe defects can instead be associated with tachyarrhythmias caused by compression (and displacement) of the right heart and pulmonary artery. There also may be a pulmonic flow murmur and a right ventricular strain pattern on electrocardiogram (ECG). Finally, the limited movements of the chest wall can cause a compensatory increase in respiratory rate and a shift toward a more diaphragmatic respiration. This, in turn, may increase the work of breathing and thus lead to greater fatigability. Abnormal drainage of secretions also may cause respiratory infections, and even asthma.

77 What is a pigeon chest?

It is the opposite of the funnel chest: a sternal protrusion from cartilage overgrowth, with forward sternal projection and secondary flattening of either side of the chest (Fig. 13-7). This makes the sternum resemble the keel of a ship (carina in Latin), and thus the term pectus carinatum. As its counterpart, a funnel chest may be isolated or associated with specific diseases, like rickets, Marfan’s, or Noonan’s. Yet, contrary to the funnel chest, a pectus carinatum is much more of a medical oddity (with prevalence of 0.06% as opposed to 1 in 300–400 births).

Figure 13-7 Pectus carinatum.

(From James EC, Corry RJ, Perry JF: Principles of Basic Surgical Practice. Philadelphia, Hanley & Belfus, 1987.)

78 What are the clinical consequences of a pigeon chest?

Usually pain, due to the forward buckling of the sternum and ribs. A pectus carinatum also produces a rigid chest, which is almost fixated near full inspiration. This, in turn, leads to pockets of hypoventilation, with increased frequency of respiratory infections and even asthma. It also creates the need for a greater use of both the diaphragm and accessory muscles of respiration, especially during strenuous exercise. Hence, the easy fatigability of these patients. Finally, in contrast to pectus excavatum, the heart of a patient with pigeon chest is normally situated, and thus there are neither murmurs nor arrhythmias.

79 What can be done to correct these conditions?

Surgery. Both conditions are amenable to surgical correction.

Abnormalities of the Ribs

81 What is the normal slope?

An oblique one, at a 45-degree angle—thus giving the thorax a 0.70–0.75 ratio between AP and transverse diameter.

82 How is the rib slope modified by disease?

In patients with emphysema, chronic bronchitis, or status asthmaticus, the excessive pull on ribs and sternum by the accessory muscles of respiration (i.e., scalene and sternocleidomastoids) may horizontalize the slope. This can become severe enough to equalize the chest’s AP and transverse diameters (or, at least, bring their ratio close to 0.90)—which, in turn, leads to a barrel chest.

83 What is a barrel chest?

A chest that is almost round, with horizontalized ribs and an equalized thoracic ratio.

84 How good is the interobserver reliability for the detection of this abnormality?

Around 70%.

85 How are the physiologic consequences of a barrel chest?

Detrimental. A horizontal rib slope may compromise lung function, making ventilation less efficient.

86 What is the clinical significance of a barrel chest?

Conventional wisdom links it to COPD, even though the evidence supporting this association is rather weak. Moreover, many emphysematous patients are so underweight that their flattened bellies may only give the illusion of an increased transverse diameter. Finally, horizontalization of the ribs (and thus a barrel chest) may simply occur as a result of aging.

87 What are the most common abnormalities in rib shape?

They are deformities caused by thickening of the costochondral junction, forming two rosary-like lines of beads across the anterior chest. Common in rickets, these are referred to as rachitic rosary.

88 What is the Harrison’s groove?

It is another rib abnormality of rickets, first described in 1820 by the English physician Edward Harrison. The groove (or sulcus) is a horizontally oriented depression at the site of diaphragmatic costal insertion, caused by the phrenic pull on ribs weakened by rickets or another bone disease. The resulting indentation extends bilaterally from the xiphoid process to the axillae, making the chest resemble the body of a violin. In addition to rickets (where Dr. Harrison first described it), the “groove” also can be seen in various pediatric conditions characterized by chronic inspiratory obstruction, like, for example, laryngeal stenosis. In this case, the mechanism is not bone softening, but excessive diaphragmatic pull on bones that, albeit normal, are pliable because of growing.

89 What is Hoover’s sign?

It is a paradoxical inspiratory movement of the lateral rib cage in patients with COPD. It has been attributed to direct traction by the flattened diaphragm on the lateral rib margins. Since the diaphragmatic contraction of these patients pulls the lower ribs toward the midline, the subcostal angle (i.e., the angle between the xiphoid process and the right or left costal margins) becomes more acute.

90 What is the normal behavior of the lower rib cage during inspiration?

Normally, the costal margins move very little during quiet respiration, but, if they do, they tend to move outward and upward. In some healthy subjects, they may even move a little inward, especially at the end of peak inspiration. This movement, however, is grossly exaggerated in patients with obstructive lung disease, with 77% of them exhibiting a large and paradoxical inward pull (Hoover’s sign).

91 Is this paradoxical inward movement also affecting the sternum?

Yes. In patients with COPD, the paradoxical motion of the rib cage can be observed not only on lateral view (as Hoover’s sign, involving the ribs), but also on the frontal plane—as a paradoxical in-drawing of the lower sternum during inspiration.

92 What is the pathophysiology of Hoover’s sign?

In his first description, Hoover attributed the paradoxical motion of the lateral rib cage to the inward pull produced by diaphragmatic contraction. Gilmartin and Gibson found that transdiaphragmatic pressure does indeed support this hypothesis. They also found a weak correlation (r = 0.36) between FEV₁ and inward displacement of the lateral rib margin. Although the mean FEV₁ of obstructive patients with or without Hoover’s was identical, the sign was significantly more frequent in patients with severe airflow obstruction. This is intuitive, since the hyperinflation of obstructive disease alters the geometry of the chest wall, especially at the level of diaphragmatic insertion. This, in turn, prevents the diaphragm from having an expanding effect on the lower ribs upon contraction. In fact, it has a retracting effect.

93 Are there any other disease states characterized by Hoover’s sign?

In addition to rickets, Hoover’s sign also can be seen in large pneumothoraces or large pleural effusions. Both conditions are similarly characterized by a flattening of the diaphragm. In these processes, however, the paradoxical inspiratory movement of the costal margin toward the midline occurs only unilaterally. Conversely, in emphysema it occurs bilaterally.

94 What is Hoover’s groove?

It is a different term for Hoover’s sign. It refers to the bilateral depression caused on the thoracic cage by the inward pulling of the flattened diaphragm. In rachitic children (where it was first described), this groove is independent of respiration, since their softened bone gets molded even by a normal diaphragmatic pull (see also Harrison’s groove). Conversely, in COPD it occurs only in inspiration.

95 What is the clinical and prognostic significance of Hoover’s sign in COPD?

It is associated with increased dyspnea—during both normal activities and exercise. It also is associated with an increased use of health care resources.

96 What is the diagnostic accuracy and observer agreement for Hoover’s sign?

A study from Spain recently addressed these issues, and found an interobserver reliability ([kappa] statistic) of 0.74 between residents and attendings, which was as good (if not even better) as the agreement for other signs of COPD, such as wheezes, rhonchi, and distant lung sounds. Hoover’s sign had an overall sensitivity for COPD of 58% and a specificity of 86%; it also had a positive likelihood ratio of 4.16, which was higher than that of the other signs (which tended to have higher specificity than sensitivity). Thus, Hoover’s sign is easy to recognize and helpful in the detection of airflow obstruction. In this same Spanish series, patients with Hoover’s sign also were heavier (as measured by body mass index) than the ones without it. Hence, obesity (and its related increase in intra-abdominal pressure) may play an additional role in causing the abnormal diaphragmatic geometry that is at the root of this sign.

97 Who was Hoover?

Charles Franklin Hoover (1865–1927) was an American pulmonologist, who graduated from Harvard, studied in Vienna and Strasburg, and then returned to his native Cleveland, where he taught at Case Western Reserve University, studied the diaphragm, and eventually described his eponymous finding in 1920. Of interest, there are two Hoover’s signs, the other being a neurologic maneuver aimed at separating organic hemiplegia from its hysteric variety—a common problem in Hoover’s time. To carry it out, the examiner places a hand under the heel of the patient’s nonparalyzed leg, and then asks the subject to raise the paralyzed leg. The pressure exercised on the examiner’s hand by the nonparalyzed heel will be much higher in true hemiplegia than in malingering or hysteria.

98 Are there any other bony abnormalities that should be observed?

In addition to the static and dynamic abnormalities of the chest cage, one also should observe whether the patient is coughing or sighing, and whether there is any pain with that. Finally, the examiner should look for abnormalities of the chest surface, and even the neck and extremities.

(6) Abnormalities of the Chest Surface

(7) Abnormalities of Extremities and Neck Veins

Clubbing

102 What is the history of this finding?

The phenomenon has fascinated physicians since its original description by Hippocrates in a patient with empyema. Interest was rekindled in the 19th century by the German Eugen Bamberger and the Frenchman Pierre Marie and by their description of hypertrophic osteoarthropathy (HOA), a frequently concomitant (but separate) disorder. By the end of World War I, both clubbing and HOA had become well-known signs of chronic infection. Today, they are more commonly remembered for their association with cancer, usually bronchogenic carcinoma. In fact, this association is so strong for HOA that it has earned it the name hypertrophic pulmonary osteoarthropathy, even though HOA is not necessarily limited to pulmonary diseases. Still, despite increased awareness and some recent interesting twists, the pathogenesis of these two conditions remains an unsolved mystery.

103 Is clubbing painful?

No. Clubbing is never painful, although at times patients may complain of an aching discomfort in their fingertips. Conversely, HOA is typically painful.

104 Is clubbing limited to fingers?

No. It usually involves both fingers and toes; however, it may involve only fingers or only toes. Moreover, it can be bilateral and symmetric, or unilateral and involving a single digit.

105 Which are the causes of “differential” clubbing?

Clubbing limited to only the hands or only the feet is usually the result of a cyanotic type of congenital heart disease that selectively sends desaturated blood to either the upper or lower half of the body. The disorders most commonly responsible for differential clubbing (and cyanosis) include (1) patent ductus arteriosus with pulmonary hypertension (in which the reversed shunt limits clubbing/cyanosis to the feet and spares the hands) and (2) right ventricular origin of the great vessels (in which the reversed shunt limits clubbing/cyanosis to the hands and spares the feet). In this last disorder, both the aorta and pulmonary artery arise from the right ventricle, often in association with a ventricular septal defect, a patent ductus arteriosus, and pulmonary hypertension. As a result, oxygenated blood from the left ventricle enters the pulmonary trunk through the septum, shunts through the patent ductus arteriosus into the descending aorta, and eventually flows to the lower extremities. Conversely, oxygen-desaturated blood from the right ventricle enters the ascending aorta and brachiocephalic vessels, thereby reaching the upper extremities. Hence, the hands will be cyanotic and clubbed, but the feet are normal (reversed differential cyanosis). Finally, identical and symmetric cyanosis/clubbing of both fingers and toes indicates instead the presence of a right-to-left intracardiac shunt.

106 What is the cause of unilateral clubbing?

Usually, an aneurysm of the aorta or innominate/subclavian arteries. Pancoast’s tumor and lymphangitis also may cause unilateral clubbing. Less common is a surgical arteriovenous fistula for dialysis.

107 What are the diagnostic features of clubbing?

They depend on whether clubbing is present alone or in association with periostosis (see HOA in questions 117–122). Clubbing without periostosis, the time-honored Hippocratic nail, has three diagnostic features (Fig. 13-8):

1. Loss of Lovibond’s angle: This is the angle between the base of the nail and its surrounding skin (hyponychial or unguophalangeal angle). The angle is normally <180 degrees. In clubbing, however, is either obliterated (straight line) or >180 degrees. The loss of the Lovibond’s angle (Fig. 13-9) can be easily visualized by resting a pencil over the nail. Normally, there should be a clear window between the pencil and the nail. In clubbing, however, there will be none. Thus, the pencil will fully rest over the nail.

2. Floating nails (ballotability of the nail bed): This refers to an increased sponginess of the soft tissue at the base of the nail. As a result, the nail plate acquires a “springy” feeling: when the skin just proximal to the nail is compressed, the nail sinks deep toward the bone; upon release, it springs backward and outward (floating fingernail base)—almost like pushing an ice cube down a pot of water. This feeling can be effectively simulated by:

Pressing your right index finger over the skin just proximal to the nail of your left middle finger. In a normal person, the nail plate feels solidly attached to the underlying bone.

Repeating the maneuver, but this time applying some tension to the nail by pulling downward its free edge with your left thumb, thereby increasing the natural convexity of the nail plate. After doing so, the nail plate will feel detached from the underlying bone, capable of sinking down during pressure and springing back upon release, almost as if it were floating on a spongy pad.

3. Abnormal phalangeal depth ratio: This consists of a greater depth of the fingertip when measured at the cuticle (distal phalangeal depth [DPD]) as compared to the interphalangeal joint (interphalangeal depth [IPD]) (see Fig. 13-10). The normal DPD/IPD ratio is, on average, 0.895, which means that the fingertip tends to taper going from the distal interphalangeal joint toward the end. Conversely, in clubbing it bulges, with a DPD/IPD ratio >1.0 (i.e., in excess of the norm by approximately 2.5 standard deviations). The DPD/IPD ratio is an excellent marker for clubbing, with good sensitivity and specificity. For example, a ratio >1.0 is found in 85% of children with cystic fibrosis and fewer than 5% of children with chronic asthma.

Figure 13-8 Diagnostic features of clubbing (Dick Ket’s self-portrait from the Museum voor Moderne Kunst, Arnhem, Holland). See text for explanation.

Figure 13-9 Measurement of Lovibond’s angle.

(Adapted from Hansen-Flaschen J, Nordberg A: Clubbing and hypertrophic osteoarthropathy. Clin Chest Med 8:287–298, 1987.)

Figure 13-10 Phalangeal depth ratio.

(Adapted from Hansen-Flaschen J, Nordberg A: Clubbing and hypertrophic osteoarthropathy. Clin Chest Med 8:287–298, 1987.)

108 Is ballotability of the nail an exclusive indication of clubbing?

No. It also may be encountered in older patients with no clubbing. Still, ballotability remains an important and valuable sign for the diagnosis of this condition.

109 How quickly can these changes occur?

Rather quickly. In a setting of lung abscess, for example, loss of the unguophalangeal angle and ballotability of the nail bed have reportedly occurred within 10 days after aspiration. Once the underlying condition has been removed, changes also can quickly disappear.

110 Is increased curvature of the nail a sign of clubbing?

Not necessarily (see below, question 116). True clubbing requires accumulation of soft tissue at the base of the nail. Hence, it is defined not by an increase in nail convexity but by the three aforementioned characteristics.

111 What is a drumstick finger?

It is one of several terms used to describe the more advanced stages of clubbing (Fig. 13-11). The accumulation of connective tissue extends well beyond the base of the nail and involves the entire digit. Depending on where this accumulation predominates, a few colorful terms have been created. For example, in parrot’s beak clubbing, the swelling is primarily localized to the proximal portion of the distal digit; in the drumstick type, it is circumferential; and in the watchglass form, swelling is mostly at the nail base.

Figure 13-11 Types of digital clubbing: A, parrot’s beak; B, watchglass, and C, drumstick.

(Adapted from Hansen-Flaschen J, Nordberg A: Clubbing and hypertrophic osteoarthropathy. Clin Chest Med 8:287–298, 1987.)

112 What is Schamroth’s sign?

It is the disappearance of the diamond-shaped window normally present when the terminal phalanges of paired digits are juxtaposed (Fig. 13-12). It is just another and more recently described maneuver to confirm the loss of the Lovibond angle. It was first reported in 1976 by the South African cardiologist Leo Schamroth, who noticed it on himself during recurrent clubbing due to bouts of endocarditis.

Figure 13-12 Schamroth’s sign.

(Adapted from Hansen-Flaschen J, Nordberg A: Clubbing and hypertrophic osteoarthropathy. Clin Chest Med 8:287–298, 1987.)

113 What is the clinical significance of clubbing?

Clubbing is a feature not only of lung disease, but also of several chronic inflammatory conditions not necessarily limited to the lungs. In fact, it has been described in infective endocarditis, lung abscess, bronchiectasis, and even amyloidosis. It also has been reported in chronic inflammatory bowel disease, such as Crohn’s and ulcerative colitis. Although described in hypercapnia (usually from chronic bronchitis), clubbing is not a feature of emphysema. It is, however, encountered in hypoxemia from shunts (either cardiogenic or pulmonary) and in patients with sex hormones imbalance (because of either pregnancy or cirrhosis). Finally, clubbing has been described in various cancers, especially lung (see Table 13-1).

Table 13-1 Disorders Commonly Associated with Digital Clubbing

* Commonly associated with hypertrophic osteoarthropathy.

(Adapted from Hansen-Flaschen J, Nordberg J: Clubbing and hypertrophic osteoarthropathy. Clin Chest Med 8:287–298, 1987.)

114 What is the pathogenesis of clubbing?

One we have recently managed to better understand. Clubbing can be secondary or primary, with the latter form including both the idiopathic and hereditary varieties (of these, familial clubbing is not unusual in African-Americans). Overall, 80% of secondary cases are due to an underlying respiratory disorder, either neoplastic or inflammatory. The rest is either cardiac or gastrointestinal in origin, with less than 10% being idiopathic or hereditary. The underlying mechanism is a fibrovascular proliferation of the nail bed, possibly triggered by the clumping of large platelets in digital vessels. These are usually filtered out by the pulmonary vasculature, but in situations of pulmonary damage (from neoplastic or inflammatory disorders) or vascular shunt (from cirrhosis, pregnancy, and intracardiac defects), they manage to reach the distal digits, where they clump, release mediators, and trigger a fibrovascular response. In cases of endocarditis or infected dialysis shunts, platelet clumps would originate directly on the damaged vascular surface, detach, and eventually lodge in the digital vessels. Clubbing also may be familial, especially in African Americans.

115 What about congenital clubbing?

Congenital clubbing is relatively common and thus important to recognize. It may be characterized more by loss of the subungual angle than by presence of ballottement. Since many patients are unaware (and may not think of it unless asked), it should be well documented in the medical record.

116 What is pseudo clubbing?

A separate sign, characterized by an overcurvature of the nails in both the longitudinal and transverse axes (“watchglass nail”) that nonetheless preserves a normal Lovibond angle. It is often accompanied by hypertrophy of the distal phalanx, making the finger resemble a drumstick (“drumstick dactylitis” or “parrot beak nail”). Ironically, pseudoclubbing may be a more frequent hallmark than clubbing of a longstanding and debilitating condition, such as carcinoma of the lung, pulmonary tuberculosis, and rheumatoid arthritis. Note that nail convexity usually takes longer to develop than true clubbing, since it requires the formation of an entirely new nail plate ridge. This transverse ridge appears 1 month after the causative event, and reaches full formation at 6 months. At completion, an entirely new nail has been created, with an abnormal and more convex profile.

Hypertrophic Osteoarthropathy (HOA)

118 Which bones are most prominently affected by the periostosis of HOA?

The diaphysis of the extremities. These include, in descending order, the radius and ulna, tibia and fibula, humerus and femur, metacarpals and metatarsals, and the proximal and middle phalanges. In addition to new bone proliferation, other diagnostic features of HOA include (1) symmetric arthritis-like changes in one or more joints (ankles, wrists, knees, and elbows); (2) coarsening of the subcutaneous tissue in the distal portions of the arms and legs (and, occasionally, the face); and (3) neurovascular changes in the hands and feet (with chronic erythema, paresthesias, and increased sweating).

119 What is the boundary between HOA and clubbing?

Fuzzy. HOA may occur in some disorders that commonly present with clubbing (thus the association), but not necessarily. For example, it can be seen in cystic fibrosis, bronchiectasis, chronic empyema, and lung abscesses (all typically associated with clubbing), while instead being rare in pulmonary interstitial fibrosis (also frequently associated with clubbing). Hence, HOA is in a league of its own.

120 Is HOA symptomatic?

Yes. In contrast to pure clubbing (which is painless), HOA is associated with aching and sometimes frank bony pain and tenderness. Moreover, the pretibial skin is shiny and often thickened and warm to touch. Autonomic manifestations also may be present, such as increased sweating, warmth, or paresthesias. Of interest, all these changes resolve with ablation (or cure) of the associated condition.

121 How is the diagnosis of HOA established?

Not by physical exam, but by bone radiography or, even better, scintigraphy. Both show typical evidence of periostosis. Physical exam may suggest the diagnosis, particularly in patients with clubbing and pretibial discomfort (whose tenderness over the long bones can be elicited by applying pressure on the wrists). Still, only the clubbing component of the syndrome is diagnosed on exam.

122 What is primary HOA?

It is a rare familial autosomal dominant disorder, often referred to as pachydermoperiostosis. About 3–5% of patients with HOA have primary HOA. Hence, the vast majority have it on a secondary basis.

123 What is pachydermoperiostosis?

From the Greek pachys (thick), derma (skin), peri (around), osteon (bone), osis (condition), this is a congenital and hereditary form of HOA characterized by digital clubbing and periosteal new bone formation (especially over the distal ends of the long bones). There also is coarsening of features, with thickening, furrowing, and oiliness of the facial forehead and skin, cutis verticis gyrate, as well as seborrheic hyperplasia (i.e., open sebaceous pores filled with plugs of sebum). In contrast to simple HOA, pachydermoperiostosis is characterized by less bony pain and greater skin changes. The syndrome is autosomal dominant, more severe in males, and with clinical evidence during adolescence.

124 What is cutis verticis gyrata (CVG)?

A descriptive term for a scalp condition characterized by thickening of the skin into convoluted folds and furrows that make it resemble a cerebrum. First described in 1843, it was labeled cutis verticis gyrata by Unna in 1907. It is probably due to increased peripheral use of testosterone, and thus almost exclusively limited to males, where it starts with puberty and may disappear with castration. It can present as either an isolated finding (rare) or in association with mental retardation, cerebral palsy, epilepsy, schizophrenia, cranial abnormalities (microcephaly), deafness, various ophthalmologic abnormalities (cataract, strabismus, blindness, retinitis pigmentosa), or a combination thereof. It is very common in institutionalized mental patients (where it’s found in 0.71–3.4% of Scottish and Swedish males, and 13.4% of the Italian male psychiatric population). Secondary cases of CVG have been described in various conditions, including pachydermoperiostosis, acromegaly, diabetes, myxedema, amyloidosis, syphilis, and some skin diseases (melanocytic nevi, hamartomas, and neurofibromas/dermatofibromas).

125 What is thyroid acropachy?

It is thickening of peripheral tissues (from the Greek acro, distal and pachys, thick), which occurs in 1% of patients with Graves’, often in association with other infiltrative manifestations, such as myxedema of the hands and feet and exophthalmos. Thyroid acropachy resembles HOA insofar as it is associated with clubbing and periosteal new bone formation, yet it preferentially involves the hands and feet rather than the long bones of the lower extremities. It also spares the joints and is usually painless. Graves’ disease is often preexistent. In fact, patients can be hypothyroid, euthyroid, or hyperthyroid.

Inspection of the Neck

127 Which areas should be paid attention to?

Primarily two:

128 What should be noted about the accessory muscles of respiration?

First of all, whether scaleni, sternocleidomastoids, and trapezii are being used; if so, whether they appear hypertrophic. Normally, only the diaphragm contracts in inspiration (expiration is mostly due to passive recoil), but in situations of increased work of breathing (as in chronic lung disease or respiratory distress), accessory muscles may be recruited. In fact, more than 90% of patients hospitalized for exacerbation of COPD exhibit some use of accessory respiratory muscles, even though this usually resolves with clinical improvement. Chronic use of these muscles eventually leads to hypertrophy.

129 What are the most important of these accessory muscles?

It depends. For inspiration, the most important are the scaleni and sternocleidomastoids; for expiration, the abdominal obliques are instead predominant. Overall, the scaleni are used before the sternocleidomastoids; both are employed in patients exhibiting retractions (Fig. 13-13).

Figure 13-13 Surface anatomy of the lateral neck region.

(From James EC, Corry RJ, Perry JF: Principles of Basic Surgical Practice. Philadelphia, Hanley & Belfus, 1987.)

130 What is the physiology of these muscles?

The sternocleidomastoids lead to an inspiratory upward motion of the clavicles (and first ribs). This may provide additional chest expansion in patients with COPD, especially those burdened with flattened diaphragms and unfavorable lung mechanics. Indeed, upward motion of the clavicle in excess of 5   mm is a valuable sign of severe obstructive disease, correlating with FEV₁ of 0.6   L. The three scalene muscles, on the other hand, connect the cervical vertebrae to the first and second ribs. Their function is to assist the intercostals in raising the rib cage.

131 What about inspiratory retractions of the suprasternal and supraclavicular fossa?

They may be seen in patients with COPD who have excessive swings in intrathoracic pressures. The mechanism is the same as for retraction of the intercostal spaces (tirage).

132 What about accessory expiratory muscles?

They primarily help exhalation (by providing an additional “push”) but also may help inspiration (by easing the inspiratory recoil that follows expiration).

133 Which neck vein abnormalities may provide clues to the diagnosis of lung disease?

134 What is the clinical value of palpation?

135 What are the main components of palpation?

Assessment of the Trachea

137 What is the value of a tracheal shift?

It reflects a mediastinal shift. And when combined with other methods of evaluation (percussion and auscultation) it also allows for its proper interpretation.

138 How do you detect a tracheal deviation?

First, ask the patient to sit up, lean forward, and keep the head straight. Then place the tip of your small finger in the fossa between the medial end of the sternocleidomastoid and the lateral aspect of the trachea (Fig. 13-14). Compare the depth of this fossa to the contralateral one. They should be symmetric. If not, the patient has a tracheal shift—typically toward the side with the smaller fossa.

Figure 13-14 Palpation of the trachea (tracheal shift).

(From James EC, Corry RJ, Perry JF: Principles of Basic Surgical Practice. Philadelphia, Hanley & Belfus, 1987.)

139 What are the possible causes of a tracheal shift?

(1) An increase in volume of the contralateral lung and/or pleural space or (2) a decrease in volume of the ipsilateral lung. The latter is usually due to atelectasis, whereas a volume increase is often the result of pneumothorax, large pleural effusion, or massive consolidation. Palpation of the trachea without the other steps of chest examination is usually unable to identify the reasons for a shift.

140 How can one distinguish tracheal deviation of lung collapse from that of effusion?

141 How do you assess for mobility of the trachea?

It depends on the mobility:

142 What is Oliver’s sign?

A downward displacement of the cricoid cartilage that coincides with each heartbeat. To better detect the “tug,” ask the patient to sit up with the head and chin extended, and then grasp the cricoid cartilage. Apply a gentle upward pressure with both the thumb and index finger. A downward tug of the trachea, synchronous with each systole, suggests the presence of an aortic arch aneurysm that overrides the left main bronchus and pulls it down at each ejection. However, the sign also can present with mediastinal tumors or even simple COPD. First described in 1878 by the British military surgeon William S. Oliver (who served mostly in India and ended his career as surgeon general): “Place the patient in the erect position, direct him to close his mouth, and elevate his chin to the fullest extent. Then grasp the cricoid cartilage between your finger and thumb, and use gentle upward pressure on it. If dilatation or aneurism exist, the aortic pulsation will be distinctly felt transmitted through the trachea to the hand.”

143 What is Cardarelli’s sign?

Another sign of aortic aneurysm, and a sort of Oliver’s sign on steroids. To elicit it, press on the thyroid cartilage, gently displacing it toward the patient’s left. This shift in the trachea increases contact between the left main bronchus and the aorta, thus making it possible for the examiner to feel a transverse pulsation of the trachea in cases of aortic arch aneurysm. First described by the Italian cardiologist Antonio Cardarelli (1831–1926).

144 What is Campbell’s sign?

A downward displacement of the thyroid cartilage during inspiration. Although also a form of tracheal tug, Campbell’s sign is not due to aortic aneurysms, but to chronic airflow obstruction. To elicit it, place the tip of your index finger over the thyroid cartilage, and look for an inspiratory descent of the trachea >2.5 inches during inspiration. This is an accurate predictor of severity of airflow obstruction, correlating well with duration of symptoms and reduction in forced expiratory volume in 1 second (FEV₁). Still, Campbell’s sign is not specific for COPD, since it is positive in other situations of acute respiratory distress. In fact, it is due to an excessive inspiratory pull on the trachea during strong diaphragmatic contraction.

145 What are laryngeal height and laryngeal descent?

Laryngeal height is the distance between the top of the thyroid cartilage and the suprasternal notch. Maximum laryngeal height is measured at end of expiration; minimum laryngeal height at end of inspiration. The difference between the two is the laryngeal descent (see Fig. 13-15).

Figure 13-15 Laryngeal height measurement (in centimeters between the black bars) reflects the degree of hyperinflation. Marked hyperinflation is present if the measurement is <4   cm.

146 What is the value of laryngeal height?

It can determine both presence and severity of airflow obstruction. In fact, a laryngeal height <4   cm is a strong predictor of postoperative pulmonary risk in patients evaluated for nonthoracic surgery. In a prospective study of 272 patients by McAlister et al., three risk factors independently predicted postoperative complications: (1) age of 65 or older; (2) smoking history of 40-pack years or more; and (3) maximum laryngeal height of 4   cm or less. The latter had a p value <0.0001. Hence, such a simple physical sign can be highly predictive of pulmonary complications. Laryngeal height also is a strong predictor of the presence of obstructive lung disease (OLD). In another study by McAlister, only four clinical factors were significantly associated with a diagnosis of OLD on multivariate analysis: (1) smoking 40-pack years or more (LR, 8.3); (2) self-reported history of chronic OLD (LR, 7.3); (3) maximum laryngeal height of 4   cm or less (LR, 2.8); and (4) age of 45 or older (LR, 1.3). Patients having all four findings had an LR of 220 (ruling in OLD); those with none had an LR of 0.13 (ruling out OLD).

147 What is the value of tracheal auscultation?

It allows for recognition of stridor (i.e., of a “wheeze” that is present only in inspiration). This should not be confused with a true wheeze, which is either expiratory, or both inspiratory and expiratory. Still, even expiratory wheezes should be considered as originating from the upper airways when they are louder over the trachea than the chest. In fact, unless the patient is morbidly obese, these sounds usually reflect expiratory adduction of the vocal cords (vocal cord dysfunction) and thus should prompt laryngoscopy in all patients presenting with “refractory asthma.” Finally, tracheal auscultation also allows for the measurement of the forced expiratory time, a valuable tool for determining the presence and severity of airflow obstruction (see Chapter 14, question 48).

Assessment of the Vocal Tactile Fremitus

148 What is the vocal tactile fremitus (VTF)?

It is the Latin term for a palpable thrill produced by the patient’s voice. This can be detected by placing the hand sequentially over various areas of the chest and by then feeling the thrill that is transmitted whenever the patient is asked to say something (Fig. 13-16). Most commonly, these sounds are “Eeee,” or “1, 2, 3,” or even “99”—all terms that have more historical than clinical values (they go back to the original German neun und neunzig [i.e., “99”]), and really matter very little, since any word or sound would probably do. And yet, it also is true that some sounds, especially the lower-pitched ones, can better pass the alveolar air filter, thus leading to a stronger tactile fremitus. This might explain why men—who have lower-pitched voices than women—have more prominent VTF.

Figure 13-16 Locations on the posterior aspect of the chest for evaluating tactile fremitus.

(Adapted from Swartz MH: Textbook of Physical Diagnosis, 3rd ed. Philadelphia, WB Saunders, 1997.)

149 What is the clinical value of the VTF?

It provides information on sound transmission. In VTF, the larynx generates the sound; this is then transmitted downward along the tracheobronchial tree, across the pleura, through the pleural cavity/chest wall, and finally up into the hand of the examiner. Any abnormality along this way may compromise transmission, thus creating a softer and less palpable thrill. For example, an obstructed distal bronchus (because of either tumor or mucous plug), a large collection of fluid or air in the pleural space, or even a thicker skin (because of adipose tissue) will all soften the fremitus. Still, the hallmark of an abnormal VTF is the difference between the two sides of the chest—the asymmetry. Thus, each side should be compared carefully, level by level. A localized increase (or decrease) in fremitus is key.

150 Can any disease increase the VTF?

Yes—for example, pneumonia. Note that the VTF varies, depending on whether the pneumonia is primarily alveolar or bronchoalveolar. If limited to the alveoli (i.e., patent bronchi surrounded by pus-filled parenchyma), the VTF will be increased, since fluids (or solids for that matter) transmit sound better than air. If the pneumonia extends instead to the bronchi (i.e., broncho-pneumonia, as typical of Haemophilus influenzae), the transmission of the VTF will be dampened by intrabronchial secretions, and thus softened. Hence, pneumonia increases the VTF only if alveolar; it decreases it if bronchoalveolar.

151 How good is agreement for VTF among physicians?

Poor. Two studies suggest that interobserver agreement is just a little better than chance. Agreement among physicians for chest findings detected by inspection also has been shown to be poor.

Assessment of Expansion of Hemithoraces

153 How do you assess hemithoracic expansion?

Stand behind the patient and grab both hemithoraces with open and extended hands. Lay your palms on the chest wall. Then ask the patient to exhale completely, while at the same time closing in with both hands and juxtaposed thumbs. On subsequent deep inspiration, your thumbs will move outward with the expanding chest, thus serving as pointers of the hemithoraces’ symmetry, synchrony, and expansion.

Other Goals of Palpation

155 How valuable is percussion?

Although less studied than auscultation, percussion remains a key component of the chest exam. Laënnec suggested that it should complement auscultation in the differential diagnosis of pleural effusion, pneumonia, pneumothorax, and emphysema—diseases in which percussion still provides crucial information (see also summary table at the end of Chapter 14).

156 What is the history of percussion?

Listening to sounds of the body (either spontaneous or elicited) was a truly revolutionary advance in physicians’ ability to make a diagnosis. Although succussion had been described by Hippocrates (and so had been percussion of the abdomen), things really took off only in 1754–1761, thanks to Auenbrugger’s work on chest percussion. They got even better 60 years later, when Laënnec, frustrated by percussion, added stethoscopy to the physician’s toolbox (see Chapter 14, question 1), yet it was Giovanni Maria Lancisi (1654–1720), Roman physician to three popes and medical historian in his own right, who first intuited (and reported) the diagnostic value of thoracic percussion.

157 Who was Auenbrugger?

Josef Leopold Auenbrugger (1722–1809) was an Austrian physician and the son of a wealthy innkeeper from Gratz. As a boy, little Josef used to follow his dad down to the family cellar and watch him percuss barrels of wine to see whether they were full or empty. All this paternal “tapping” must have triggered something in Auenbrugger’s adolescent brain because years later, while working as an unpaid volunteer at the Spanish Military Hospital of Vienna, he concocted the cockamamy idea that human chests might similarly yield important clues about their content, thus allowing pathologic diagnoses without a need for autopsy. This novel thought was probably rooted in Auenbrugger’s musical interests (he was a part-time musician, who could readily discriminate between slight changes in pitch and who later even wrote a libretto for Antonio Salieri—Mozart’s menace in Peter Schaffer’s Amadeus). Whatever the reason, Auenbrugger spent 7 years at the Spanish Military Hospital of Vienna, observing changes in sound caused by various lung or heart diseases, validating his findings with both autopsies and experiments, and even testing his sound-muffling theories by percussing variously filled barrels and cadavers. After all this cataloging, tapping, and studying, he finally published his observations in 1761, the same year Morgagni published his three-volume masterpiece of clinico-pathological correlation. Auenbrugger’s opus was instead a mere 95 pages, written in Latin, and bearing the concise title, A New Discovery that Enables the Physician from the Percussion of the Human Thorax to Detect the Diseases Hidden Within the Chest. In this unassuming booklet, 39-year-old Auenbrugger described the various chest tones, ranging from normal (resembling that of a drum) to those produced by various thoracic diseases: (1) the sonus altior (high or tympanic sound); (2) the sonus obscurior (indistinct sound); and (3) the sonus carnis percussae (dull sound). He then concluded it all by announcing that simple percussion could provide physicians with pathologic information in the live patient that up to that point had been the prerogative of autopsies. It was a breakthrough. Because of this, and the work carried out in the Spanish hospital, Empress Maria Theresa eventually ordered the Viennese Faculty of Medicine to admit him at no charge as a full member. Yet, as often happens to major scientific revolutions, his little book produced a whimper and not a bang. Some even ridiculed it. Percussion remained largely underutilized and a sort of medical oddity until 50 years later, when baron Jean-Nicolas Corvisart des Marest, academician extraordinaire and personal physician to Napoleon, stumbled upon it while reading a book by Stoll, former director of the Spanish Military Hospital of Vienna. Corvisart got so intrigued by Auenbrugger’s discovery, that he studied it for years and soon started teaching it to his own students. Eventually, he became so enamored with this technique as to use it regularly on rounds, predicting with remarkable and theatrical accuracy the inevitable autopsy findings. It must have been all these predictions, or Corvisart’s fame, or his 1808 translation of the Inventum Novum (the year before Auenbrugger’s death), but eventually percussion became the royal road to bedside diagnosis—“royal” until one of Corvisart’s unsatisfied students (a diminutive and introverted Breton, named René Théophile Hyacinthe Laënnec) developed auscultation. The rest, as they say, is history.

158 What is the physics behind percussion?

It is the physics of the delivery of a fixed amount of energy to the chest wall and its back reflection as sound. The characteristics of this soundwave (amplitude and frequency) are inversely related, whereas their product remains constant. What determines these characteristics, however, remains controversial. One school of thought considers them dependent on the underlying percussed tissues. Thus, the reflected sound would have either high frequency/low amplitude or low frequency/high amplitude, based on the type of tissue percussed. In other words:

Hence, if the strength of striking and chest wall thickness remain constant, the relative pitch of the percussion note will depend on the ratio between aerated tissue/solid or liquid medium (Table 13-2 and Table 13-3).

Table 13-3 Summary of Features of the Percussion Note

Yet another theory argues that the entire chest cage (not only the underlying tissues) resonates in response to percussion and creates the soundwave. In this sense, topographic percussion would be basically impossible, since even distant organs would participate in the sound production.

Percussion Techniques

160 What is the current role of direct percussion?

It is still used at times for a quick screening. One form of direct percussion, for example, relies on the clavicles as pleximeters for the assessment of lung apices.

161 What is mediated or “indirect” percussion?

A technique developed in 1828 by the French Piorry, another of Corvisart’s students and himself the inventor of “topographic” percussion—a way to map out the borders of various organs through sound. Mediated percussion consisted of percussing the chest—not directly—but through a solid body applied to the wall. This mediator, called a pleximeter, was to be struck with a small hammer. Piorry had initially tried lead, leather, horn, and wood but eventually settled on ivory, manufacturing a little disc that “had to be” 5   cm in diameter and 2.5   mm in thickness. Despite these guidelines, cheaper pleximeters (usually in wood) immediately flooded the market. To avoid their common loss, many of these gadgets became screwed to the end of one of Laënnec’s stethoscopes. If all was lost (literally), a coin provided an easy substitute. Finally, the British William Stokes and James Hope, who had listened to Piorry’s lessons in Paris (and who must have lost their pleximeters quite often), simplified the method by using instead their own middle fingers (no offense implied). Although disliked by Piorry, this variation eventually became the standard, thanks primarily to Skoda, who had become the chief advocate of mediated percussion in Vienna, and also the author responsible for the four major types of percussion note still taught today.

162 What is the current technique for indirect percussion?

It consists of laying the pleximeter finger (usually the middle digit of the left hand in right-handed examiners) onto the intercostal space between two ribs (and not on the rib, to avoid transforming it into a pleximeter itself, thus spreading the sound). To avoid dampening vibrations, only the distal interphalangeal joint of the extended pleximeter finger is allowed to touch the skin. The rest (and all other fingers) are instead lifted off the chest wall. The blow is then delivered via the middle finger of the opposite hand, flexed like a hammer at a 90-degree angle, and brought down over the distal interphalangeal joint of the pleximeter finger. The blow should be strong, but not too strong (to avoid setting into vibration more distant organs). In fact, a gentler tap allows better detection of the percussion note (and also a “tactile” perception of the note). This tap should be delivered by using the wrist (and not the elbow) as a fulcrum. Once delivered, the percussing finger should be lifted from the pleximeter, to avoid any sound-dampening, even though data indicate that this might not really be necessary.

163 What is the current value of indirect percussion?

Good but limited. The following should be kept in mind:

164 Are there differences between the percussion note of lung collapse from effusion and consolidation from pneumonia?

Theoretically, yes; practically, no. In fact, this difference may be more tactile than auscultatory. In other words, the vibration “felt” by the pleximeter finger may be different depending on the characteristics of the tissue percussed. This may be intuitive for an air-filled versus a fluid-filled tissue, but it might even play a role in cases of solid tissue due to consolidation (i.e., dull), versus solid tissue due to lung compression from pleural effusion (i.e., flat). In this regard, Osler used to write, “the dullness of a pleural effusion has a peculiarly resistant, wooden quality, which is different from that of pneumonia and that can be readily recognized by skilled fingers.” With all due respect for Sir William and his insistence on the role of the tactile sense in percussion, our ability to differentiate dull from flat by palpation is frustratingly limited at best.

165 What is the current role for topographic percussion?

Indirect percussion of the “topographic” type is mostly used to map out diaphragmatic excursion, since it has tremendous interobserver variability, making it unsuitable for defining organ borders. To map out diaphragmatic excursion, the patient’s chest is percussed posteriorly, downward, and along the mid-scapular line until dullness is finally encountered. The patient is then asked to hold a deep breath while percussion is resumed. In the normal individual, there will be an additional 3–6   cm of resonance, indicative of the normal diaphragmatic movement. In situations of lung disease (or diaphragmatic paralysis), this excursion is either reduced or eliminated. In patients with COPD (whose lungs are overexpanded), diaphragmatic excursion can be limited to <2   cm. This finding has excellent specificity for COPD (>90%) but such a poor sensitivity (around 10%) to make it clinically useless.

166 What is auscultatory percussion?

It is a modified variety of “topographic” percussion, developed in 1940 by Camman and Clark and recently rediscovered by John Guarino as an alternative to “comparative” percussion. In either mode, detection of elicited sounds is not entrusted upon the unaided ear, but on the stethoscope.

167 Is there a role for auscultatory percussion in the detection of pleural effusion?

Yes. In fact, in its original form auscultatory percussion was advocated for the detection of pleural effusion. To do so, the patient has to be seated and the stethoscope placed in the back, 3   cm below the 12th rib. The chest is then percussed downward and posteriorly, from the apex to the base. A change in percussion note from dull to loud that is localized over the 12th rib indicates the presence of pleural fluid. In contrast to other more traditional modalities of percussion, this auscultatory variety has the same excellent sensitivity for pleural effusion (>90%), but better specificity (also >90%), being usually negative in pneumonia or atelectasis. Conversely, in its newer and revised modality, auscultatory percussion is practiced a little differently (Fig. 13-17). The physician taps lightly with the distal tip of one finger over the manubrium of the sternum (and thus anteriorly), while at the same time listening with the stethoscope over symmetric locations of the posterior chest wall. The theory is that sound so generated travels unimpeded through the lungs, reaching the opposite chest wall in a symmetric fashion. Thus, any asymmetry in sound intensity is considered a sign of lung disease. By using this technique, Guarino was able to detect pulmonary lesions <2   cm in diameter (which are almost impossible to identify with conventional percussion). Studies to confirm this technique, however, have produced conflicting results.

Figure 13-17 Method of auscultatory percussion.

(Adapted from Guarino JR. Lancet 1:1332–1334, 1980.)