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7—SELECTED PULMONARY DISORDERS
II. The Findings
Most of the traditional findings of chronic obstructive pulmonary disease (COPD) result from a
hyperinflated chest and the great effort necessary to move air across obstructed airways. Some of
these physical signs are discussed in other chapters: asynchronous breathing (Chapter 19); barrel
chest, pursed-lip breathing, and accessory muscle use (Chapter 28); hyperresonance to percussion
(Chapter 29); pulsus paradoxus (Chapter 15); diminished breath sounds and whee zing (Chapter 30),
and prolonged forced expiratory times (Chapter 31).
Additional findings are discussed below.
A. INSPECTION
1. Inspiratory Recession of Supraclavicular Fossa
and Intercostal Spaces
Some patients with respiratory distress from obstructive lung disease have recession or indrawing
of the soft tissues of the intercostal spaces and supraclavicular fossa. is finding is attributed to
vigorous breathing efforts and excess inspiratory resistance, which introduces a delay between the
generation of large negative pleural pressures and subsequent increase in lung volume (see also
Chapter 28).
2. Costal Paradox (Hoover sign, Costal Margin Paradox)
e costal paradox is an abnormal movement of the costal angle, which is the angle formed by
both costal margins as they approach the xiphoid process on the anterior body wall. e clinician
assesses costal movements by placing his or her hands on each costal margin and observing how
the hands move with respect to each other as the patient breathes. In a normal person, inspiration
causes the lateral aspects of the lower ribs to move outward, like the handle of a bucket, and the
clinician’s hands separate as the costal angle widens. In patients with the costal paradox, in contrast, the hyperinflated chest can expand no further and the flattened diaphragm instead pulls the
costal margins and the clinician’s hands together. An excellent video of the Hoover sign appears
in reference 8.
7
3. Leaning Forward on Arms Propped up on Knees
Many patients with obstructive disease experience prompt relief of their dyspnea if they lean forward, which allows them to generate greater inspiratory force with fewer accessory muscles. is
position probably diminishes dyspnea because it compresses the abdominal contents and pushes
the diaphragm upward, helping restore the normal domed appearance necessary for efficient and
strong inspiratory movements.
B. PALPATION: LARYNGEAL HEIGHT AND DESCENT
According to traditional teachings, the distance between the thyroid cartilage and suprasternal notch (laryngeal height or tracheal length) is shorter in obstructive lung disease than in
normal persons, because the clavicles and sternum are positioned abnormally high. (See the
section on Barrel Chest in Chapter 28.) Patients with severe obstruction also have more forceful diaphragmatic contractions that, although ineffective in moving large amounts of air, may
pull the trachea abnormally downward during inspiration (laryngeal descent, tracheal descent, or
tracheal tug).
9,10
33—CHRONIC OBSTRUCTIVE LUNG DISEASE
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281
III. Clinical Significance
A. INDIVIDUAL FINDINGS
EBM Box 33.1 shows that several findings increase the probability of obstructive lung disease:
early inspiratory crackles (likelihood ratio [LR] = 14.6), absence of cardiac dullness (LR = 11.8),
breath sound score of 9 or less (LR = 10.2), subxiphoid cardiac impulse (LR = 7.4), hyperresonance of the chest (LR = 7.3), forced expiratory time of 9 seconds or less (LR = 3.9), reduced
breath sounds (i.e., overall impression without use of the breath sound score, LR = 3.5), use of the
scalene or sternocleidomastoid muscles during inspiration (LR = 3.3), and pursed-lip breathing
(LR = 2.7). Among patients with known obstructive lung disease, early inspiratory crackles imply
that the disease is severe (i.e., forced expiratory volume in 1 sec [FEV1]/forced vital capacity
[FVC] < 0.44; LR = 20.8).19 e simple presence of crackles without reference to their timing is
diagnostically unhelpful (LR not significant).
EBM BOX 33.1 Chronic Obstructive Pulmonary Disease*
Finding (Reference)
Barrel chest
AP/L chest diameter ratio ≥0.9
Pursed-lip breathing
Scalene/sternocleidomastoid muscle use1139 88 3.3 0.7
Maximum laryngeal height ≤4 cm
Laryngeal descent >3 cm
Hoover sign
Palpation
Subxiphoid cardiac impulse
Percussion
Absent cardiac dullness left lower sternal
border
5
Hyperresonance of chest
Diaphragm excursion percussed <2 cm
Auscultation
Reduced breath sounds
Breath sound score
≤9 23–46 96–97 10.2 …
10–12 34–63 … 3.6 …
13–15 11–16 … NS …
≥16 3–10 33–34 0.1 …
Early inspiratory crackles
Any unforced wheeze
Ancillary tests
Forced expiratory time
≥9 seconds 5–50 86–99 3.9 …
3–9 seconds 42–94 … NS …
<3 seconds 1–10 26–89 0.2 …
Combined findings
2 out of the following 3 findings present:
(1) smoked 70 pack years or more;
(2) self-reported history of chronic
bronchitis or emphysema, (3)
diminished breath sounds (5)
†
11
11
11
12
12
13
5,6
5,14
5,11,13–15
16,17
18,19
5,6,12–14,20,21
21–24
6,14
Likelihood Ratio‡
Sensitivity
(%)
Specificity
(%)
if Finding Is
Present Absent
65 58 1.5 0.6
31 84 2.0 NS
58 78 2.7 0.5
36 90 3.6 0.7
17 80 NS NS
58 86 4.2 0.5
4–27 97–99 7.4 NS
15 99 11.8 NS
21–33 94–98 7.3 0.8
5
13 98 NS NS
29–82 63–96 3.5 0.5
25–77 97–98 14.6 NS
13–56 86–99 2.6 0.8
67 97 25.7 0.3
(continued)
282
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Absent cardiac dullness,
Accessory muscle use
Forced expiratory time <3
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7—SELECTED PULMONARY DISORDERS
EBM BOX 33.1 Chronic Obstructive Pulmonary Disease*–Cont’d
*Diagnostic standards: for chronic obstructive lung disease, FEV1/FVC ratio <0.6–0.7 (palpation,
percussion, diminished breath sounds, and combined findings), FEV1/FVC <0.7–0.75 (inspection,
crackles, wheezes, and forced expiratory time), or FEV1 <40% predicted (breath sound score).
†
Definition of finding: for maximal laryngeal height, distance between the top of the thyroid cartilage and
suprasternal notch at the end of expiration; for laryngeal descent, difference in laryngeal height between
end inspiration and end expiration; for Hoover sign, paradoxical indrawing of the lateral rib margin during
inspiration, noted when the patient is standing; for hyperresonance of chest, upper right anterior chest5 or
undefined location14; for breath sound score, see Chapter 30; for forced expiratory time, see Chapter 31.
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
AP/L, Anteroposterior/lateral; cm, centimeters; FEV1, forced expiratory volume in 1 second; FVC, forced
vital capacity; NS, not significant.
LRs
Breath sound score ≥16
=
Only two findings significantly decrease the probability of obstructive disease: a breath sound
score of 16 or more (LR = 0.1) and a forced expiratory time less than 3
e evidence supporting the chest wall signs of obstructive lung disease is meager and conflicting. (See also the section on Barrel Chest in Chapter 28.) One study showed that indrawing of
the soft tissues correlated with severity of obstruction,
of adults presenting to the emergency department with significant dyspnea demonstrated that
suprasternal retractions (LR = 4) and intercostal retractions (LR = 2.2) increased probability of
hypercapnia and respiratory acidosis (but in this study only 57% had obstructive lung disease [see
=
Chapter 28]).
height of 4
cm or less (LR
other studies these signs correlated poorly with measures of obstruction.
0.9 or more increases probability of obstructive disease slightly (LR = 2). e degree of laryngeal
descent is unhelpful (LR not significant).
e chest excursion of patients with obstructive disease (mean, 3 to 4 cm, measured as change
in circumference between maximum inspiration and maximum expiration using a tape measure
at the level of the fourth intercostal space) is less than that of normal persons (mean, 6 to 7 cm),
but the lower limit observed in normal persons (2 to 3 cm) makes it impossible to draw significant
conclusions in a single person.
s
Probability
Hyperesonant chest
Hoover sign
Forced expiratory time ≥9 s
Maximum laryngeal height ≤4 cm
Diminished breath sounds
25
while another did not.
+45%+30%+15%–15%–30%–45%
LRs
Early inspiratory
crackles
left lower sternal border
Breath sound score ≤9
Subxiphoid cardiac impulse
seconds (LR
26
Another study
25,28
A thoracic ratio of
0.2).
Decrease Increase
0.1 0.2 0.5 12510
27
In two studies, Hoover sign (LR = 4.2, EBM Box 33.1) and maximum laryngeal
3.6) increased the probability of obstructive lung disease, but in two
28,29
33—CHRONIC OBSTRUCTIVE LUNG DISEASE
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283
EBM BOX 33.2 Prognosis in COPD Exacerbation: the BAP-65 Score
Mechanical ventilation
or hospital mortality
BAP-65 Class Definition*
1 0 BAP predictors present, age ≤65 years 1.6 0.3
2 0 BAP predictors present, age >65 years 2.6 0.4
3 1 BAP predictors present 6.1 NS
4 2 BAP predictors present 19.5 3.7
5 3 BAP predictors present 34.5 9.0
*“BAP predictors” include (1) Blood urea nitrogen >25 mg/dL, (2) Altered mental status (disoriented or
Glasgow coma scale <14), and (3) Pulse ≥110 beats/min.
COPD, Chronic obstructive pulmonary disease; NS, not significant.
PROGNOSIS IN COPD: BAP-65 SCORE
Probability
Decrease Increase
LRs
0.1 0.2 0.5 12510
BAP-65 score of 1
BAP-65 score of 4
% Likelihood Ratio
+45%+30%+15%–15%–30%–45%
BAP-65 score of 5
30–32
LRs
B. COMBINED FINDINGS
Of the many successful diagnostic schemes that combine findings,
three questions: (1) Has the patient smoked more than 70 pack-years? (2) Has the patient been
previously diagnosed with chronic bronchitis or emphysema? and (3) Are breath sounds dimin-
ished in intensity? Answering “yes” to two or three of these questions is a compelling argument
for obstructive disease (LR = 25.7, EBM Box 33.1).
Although using the self-reported history of emphysema as a diagnostic indicator seems to be a circular argument, the specificity of this question is only 74%, which means that 26% of patients without
obstructive lung disease actually remembered such a history. is question is more discriminatory than
other symptoms (i.e., dyspnea, sputum production, age, or use of theophylline, steroids, inhalers, or home
oxygen) and many other findings (i.e., hyperresonant chest, absence of cardiac dullness, and wheezes).
15,21
one of the simplest asks just
5
C. PROGNOSIS IN COPD EXACERBATION (BAP-65 SCORE)
In studies of more than 120,000 patients hospitalized with COPD exacerbation, three clinical findings
accurately predict the risk of mechanical ventilation or hospital mortality (overall risk for these complications was 3% to 11%): (1) Blood urea nitrogen of more than 25 mg/dL, (2) Altered mental status,
and (3) Pulse of 110/min or higher (the mnemonic “BAP”* helps clinicians recall these findings).30
Based on the number of these findings and the patient’s age, the patient can be classified into one of
five prognostic groups, as defined in EBM Box 33.2. is class, in turn, stratifies the patient’s risk of
mortality or mechanical ventilation from 1.6% to 34.5% (LRs 0.3 to 9; see EBM Box 33.2).
Despite its similarities to the CURB-65 score (see Chapter 32), the BAP-65 score is slightly
more accurate in predicting need for mechanical ventilation in patients with COPD exacerbations
than the CURB-65 score.
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
*BAP is an acronym for Blood urea nitrogen, Altered mental status, and Pulse.
33
References
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1. Rosenblatt MB. Emphysema in the nineteenth century. Bull Hist Med. 1969;43(6):533–552.
2. Osler W. e Principles and Practice of Medicine (Facsimile by Classics of Medicine Library). D Appleton and
Co.; 1892.
3. Snider GL. Emphysema: the first two centuries–and beyond. A historical overview, with suggestions for
future research: part 1. Am Rev Respir Dis. 1992;146(5 Pt 1):1334–1344.
4. Cabot R. Physical Diagnosis of Diseases of the Chest. William Wood; 1900.
5. Badgett RG, Tanaka DJ, Hunt DK, etal. Can moderate chronic obstructive pulmonary disease be diag-
nosed by historical and physical findings alone? Am J Med. 1993;94(2):188–196.
6. Holleman DR, Simel DL, Goldberg JS. Diagnosis of obstructive airways disease from the clinical exami-
nation. J Gen Intern Med. 1993;8(2):63–68.
7. Stubbing DG. Physical signs in the evaluation of patients with chronic obstructive pulmonary disease.
Pract Cardiol. 1984;10(2):114–120.
8. Lemyze M, Bart F. Hoover sign. CMAJ. 2011;183(2):E133.
J
9. Sharp
10. O’Neill S, McCarthy DS. Postural relief of dyspnoea in severe chronic airflow limitation: relationship to
11. de Mattos WL, Signori LGH, Borges FK, Bergamin JA, Machado V. Accuracy of clinical examination
12. Straus
13. Garcia-Pachon E. Paradoxical movement of the lateral rib margin (Hoover sign) for detecting obstruc-
14. Oshaug K, Halvorsen PA, Melbye H. Should chest examination be reinstated in the early diagnosis of
15. Holleman
16. Pardee NE, Martin CJ, Morgan EH. A test of the practical value of estimating breath sound intensity:
17. Bohadana AB, Peslin R, Uffholtz H. Breath sounds in the clinical assessment of airflow obstruction.
18. Bettencourt PE, Del Bono EA, Spiegelman D, Hertzmark E, Murphy Jr. RL. Clinical utility of chest
19. Nath AR, Capel LH. Inspiratory crackles—early and late. orax. 1974;29(2):223–227.
20. Marini JJ, Pierson DJ, Hudson LD, Lakshminarayan S. e significance of wheezing in chronic airflow
21. Straus
22. Lal
23. Schapira RM, Schapira MM, Funahashi A, McAuliffe TL, Varkey B. e value of the forced expiratory
24. Aggarwal AN, Das S, Agarwal R, Singh N. Utility of forced expiratory time as a screening tool for iden-
25. Godfrey S, Edwards RHT, Campbell EJM, Newton-Howes J. Clinical and physiological associations of
26. Stubbing DG, Mathur PN, Roberts RS, Campbell EJM. Some physical signs in patients with chronic
27. Zorrilla-Riveiro
JT, Drutz WS, Moisan T, Foster J, Machnach W. Postural relief of dyspnea in severe chronic
obstructive pulmonary disease. Am Rev Respir Dis. 1980;122(2):201–211.
respiratory muscle strength. orax. 1983;38(8):595–600.
findings in the diagnosis of COPD. J Bras Pneumol. 2009;35(5):404–408.
SE, McAlister FA, Sackett DL, Deeks JJ. e accuracy of patient history, wheezing, and
laryngeal
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tive airway disease. Chest. 2002;122(2):651–655.
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breath sounds related to measured ventilatory function. Chest. 1976;70(3):341–344.
orax. 1978;33(3):345–351.
auscultation in common pulmonary diseases. Am J Respir Crit Care Med. 1994;150(5 Pt 1):1291–1297.
obstruction. Am Rev Respir Dis. 1979;120(5):1069–1072.
reliability of the examination-chronic obstructive airways disease. Accuracy of history, wheezing, and
forced
2002;17(9):684–688.
Br Med J. 1964;1(5386):814–817.
time in the physical diagnosis of obstructive airways disease. JAMA. 1993;270(6):731–736.
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some physical signs observed in patients with chronic airways obstruction. orax. 1970;25(3):285–287.
airflow obstruction. Am Rev Respir Dis. 1982;125(5):549–552.
Fernández R. Nasal flaring as a clinical sign of respiratory acidosis in patients with dyspnea. Am J Emerg
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measurements in diagnosing obstructive airway disease. (CARE-COAD1 group).
DR, Simel DL. Does the clinical examination predict airflow limitation?
S, McAlister FA, Sackett DL, Deeks JJ, CARE-COAD2 group Clinical assessment of the
expiratory time in the diagnosis of chronic obstructive pulmonary disease.
S, Ferguson AD, Campbell EJM. Forced expiratory time: a simple test for airways obstruction.
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disease. Ann Intern Med. 1965;62(3):477–485.
29. Pierce JA, Ebert RV. e barrel deformity of the chest, the senile lung and obstructive pulmonary emphy-
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30. Tabak YP, Sun X, Johannes RS, Gupta V, Shorr AF. Mortality and need for mechanical ventilation in
acute exacerbations of chronic obstructive pulmonary disease: development and validation of a simple
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31. Shorr AF, Sun X, Johannes RS, Yaitanes A, Tabak YP. Validation of a novel risk score for severity of illness
in acute exacerbations of COPD. Chest. 2011;140(5):1177–1183.
32. Germini F, Veronese G, Marcucci M, etal. Validation of the BAP-65 score for prediction of in-hospital
death or use of mechanical ventilation in patients presenting to the emergency department with an
acute exacerbation of COPD: a retrospective multi-center study from the Italian Society of Emergency
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33. Shorr AF, Sun X, Johannes RS, Derby KG, Tabak YP. Predicting the need for mechanical ventilation in
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284.e2
CHAPTER
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34
Pulmonary Embolism
KEY TEACHING POINTS
• In patients with suspected pulmonary embolism the principal role of bedside examination
is to identify the patient’s overall probability of disease.
• Some individual physical findings increase probability of pulmonary embolism—
respiratory rate >30/min, unilateral calf swelling, and parasternal heave—but these
findings are infrequent and the increase in probability is modest.
• By using well-validated scores (e.g., Wells Score, revised Geneva score), clinicians can
combine risk factors and clinical findings to accurately distinguish patients with low,
intermediate, or high probability of pulmonary embolism. This information, combined with
quantitative D-dimer measurements or other structured rules, identifies which patients require
definitive testing using computed tomography (or ventilation-perfusion lung scanning).
I. Introduction
e diagnosis of pulmonary embolism is a difficult challenge that has frustrated clinicians for
over a century. In up to half of hospitalized patients who die of pulmonary embolism, for example,
the diagnosis is not even considered.
role of bedside examination is to determine the patient’s overall probability of disease (i.e., low,
intermediate, or high probability). is information, in turn, often combined with quantitative
D-dimer levels or other structured rules, is used to select which patients should undergo definitive
diagnostic testing for thromboembolism by computed tomography (CT) angiography, compression venous ultrasonography, or ventilation-perfusion lung scanning.
1,2
When pulmonary embolism is suspected, the principal
II. The Findings
Patients with pulmonary embolism present with dyspnea (61% to 83% of patients), pleuritic chest pain
(40% to 48% of patients), hemoptysis (5% to 22% of patients), or syncope (4% to 26% of patients).
Syncope is more common (affecting 20% to 80% of patients) when pulmonary embolism is massive,
meaning that it obstructs more than half of the pulmonary circulation.
patients report a prior history of thromboembolism, and 33% to 42% report calf or thigh pain.
In recent years, several investigators using multivariate analysis have identified combinations
of bedside findings that best identify a patient’s overall probability of pulmonary embolism. Two
widely studied scores are the Wells Score (Table 34.1)14 and the revised Geneva score
(Table 34.2).
*e original Geneva score
which is often unavailable. Another simplified Geneva score
has the revised score but only 1 point applied to each variable; this simplified score is less well studied.
15
* For each of these scores, the clinician simply adds the points corresponding to
8
was later revised (i.e., “revised Geneva score”) to remove the arterial blood gas analysis,
11–13
Ten percent to 35% of
45
that has been developed with the same variables
3,5–9
3–10
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7—SELECTED PULMONARY DISORDERS
TABLE 34.1 ■ Wells Score for Pulmonary Embolism
Characteristic Points
Risk factors
Previous pulmonary embolism or deep venous thrombosis 1.5
Immobilization or surgery in the previous 4 weeks 1.5
Cancer 1
Clinical findings
Hemoptysis 1
Heart rate >100/min 1.5
Clinical signs of deep venous thrombosis 3
Other
Alternative diagnosis is less likely than pulmonary embolism 3
Based upon reference 14.
Interpretation of total score: 0–1 points, low probability; 2–6 points, moderate probability; 7 or more points, high
probability.
TABLE 34.2 ■ Revised Geneva Score for Pulmonary Embolism
Characteristic Points
Risk factors
Age >65 years 1
Previous pulmonary embolism or deep venous thrombosis 3
Surgery (under general anesthesia) or fracture (of lower limbs) within 1 month 2
Cancer (active or considered cured <1 year) 2
Clinical findings
Unilateral leg pain 3
Hemoptysis 2
Heart rate
75–94 beats/min 3
≥95 beats/min 5
Pain on palpation of lower-limb deep veins and unilateral edema 4
Based upon reference 15.
Interpretation of total score: 0–3 points, low probability; 4–10 points, moderate probability; ≥11 points, high
probability.
each of the independent predictors that are present. e total score determines overall probability,
as defined in the footnotes to Tables 34.1 and 34.2. Both scores combine similar risk factors (prior
thromboembolism, immobilization, surgery, and cancer) and clinical findings (hemoptysis, tachycardia, and signs of deep venous thrombosis) to arrive at overall clinical probability, although the
Wells score also considers whether an alternative diagnosis is less likely than pulmonary
embolism.
III. Clinical Significance
A. INDIVIDUAL FINDINGS
e studies included in EBM Box 34.1 enrolled over 5000 patients with suspected pulmonary embolism referred to centers having considerable experience with venous thromboembolism. In these studies, only 1 of 5 patients suspected of pulmonary embolism actually had the
diagnosis.
34—PULMONARY EMBOLISM
LRs
PULMONARY EMBOLISM
y
Left parasternal heave
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EBM BOX 34.1 Pulmonary Embolism*
Likelihood Ratio‡
if Finding Is
Present Absent
Finding (Reference)
†
Sensitivity
(%)
Specificity
(%)
Individual findings
General description
Diaphoresis
Cyanosis
Vital signs
Pulse >100/min
Systolic blood pressure ≤100 mm Hg
Temperature >38°C
Respiratory rate >30/min
Lung
Accessory muscle use
Crackles
Wheezes
Pleural friction rub
Heart
Elevated neck veins
Left parasternal heave
Loud P
New gallop (S3 or S4)
Other
Chest wall tenderness
Unilateral calf pain or swelling
Combined findings
Wells score
9
4,9
6–10,16–18
4,6–9
8
3,9,19
6,9,19
3,9
2
7,17,22–31
4
4,9
4,9,19
4,9
3
4,20
5–7,9,10,17–19,21
4 94 NS NS
1–3 97–100 NS NS
22–43 66–91 1.4 NS
8
8 95 1.9 NS
1–9 78–98 0.5 NS
21 90 2.0 0.9
17 89 NS NS
21–59 45–82 NS NS
3–31 68–91 0.4 NS
1–14 91–99 NS NS
3–14 92–96 1.7 NS
1–5 98–99 2.4 NS
15–19 84–95 NS NS
30 89 NS NS
11–17 79–80 NS NS
9–52 77–99 2.9 0.8
Low probability, 0–1 points 6–53 27–54 0.3 …
Moderate probability, 2–6 points 38–72 … 1.6 …
High probability, 7 or more points 7–54 90–100 8.2 …
Revised Geneva Score
15,17,26–29,32
Low probability, 0–3 points 1–27 43–85 0.4 …
Moderate probability, 4–10 points 57–69 … NS …
High probability, ≥11 points 10–42 92–99 5.9 …
287
*Diagnostic standard: for pulmonary embolism, pulmonary angiography, computed tomographic
angiography, or ventilation-perfusion scanning (± compression venous ultrasonography). In 11
15,17,18,20,22,23,25,27,29,30,32
studies
were not fully tested but instead followed for at least 3 months without anticoagulation.
†
Definition of findings: for Wells Score and Revised Geneva Score, see Tables 34.1 and 34.2.
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
NS, Not significant.
Wells score, low probability
Revised Geneva score, low
some patients with low clinical risk and negative quantitative D-dimer tests
Probability
Decrease Increase
+45%+30%+15%–15%–30%–45%
0.1 0.2 0.5 12510
LRs
Wells score, high probabilit
probability
Wheezes
Revised Geneva score, high
probability
Unilateral calf pain or swelling
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7—SELECTED PULMONARY DISORDERS
Very few individual findings help the clinician distinguish patients with pulmonary embolism
from those without it. e only individual symptoms increasing probability of pulmonary embolism are sudden dyspnea (likelihood ratio [LR] = 2.4),
(LR = 1.9)
3–10,17,18
†
6,7
syncope (LR = 2),
4–6
and hemoptysis
e individual physical findings that increase the probability of pulmonary embolism are uni-
lateral calf pain or swelling (LR = 2.9; see EBM Box 34.1), left parasternal heave (LR = 2.4),
respiratory rate of more than 30 breaths/min (LR = 2), and systolic blood pressure 100 mm Hg
or less (LR = 1.9). e presence of wheezes (LR = 0.4) and fever higher than 38°C (LR = 0.5)
modestly decrease the probability of pulmonary embolism. e presence or absence of a pulse rate
of more than 100/min as an isolated finding is unhelpful (LR = 1.4), although in one study the
finding of a pulse less than 90/min decreased probability of pulmonary embolism (LR = 0.3).
3
Other individual findings are unhelpful. Chest wall tenderness is found in 11% to 17% of
patients in pulmonary embolism and has an LR that is not significant, emphasizing that this sign
is not diagnostic of costochondritis (see Chapter 29). e presence of hypoxemia, defined either as
room air pO2 less than 80 mm Hg or as increased alveolar-arterial gradient, is also diagnostically
unhelpful (both LRs not significant).
3,8,9,33
B. COMBINING FINDINGS TO DETERMINE CLINICAL PROBABILITY
OF EMBOLISM
In contrast to the modest accuracy of individual findings, EBM Box 34.1 indicates that a deter-
mination of “high probability” by either the Wells score (LR = 8.2) or revised Geneva score
(LR = 5.9) markedly increases the probability of pulmonary embolism, whereas a determination
of “low probability” by either score decreases it (LRs = 0.3 to 0.4).
Both scores emphasize that accurate assessment of a patient’s probability combines both risk
factors and clinical findings. e probability of embolism is high if the patient has typical signs
(e.g., tachycardia, leg swelling) and risk factors (e.g., cancer, immobilization) and lacks an alternative diagnosis. e probability is low if the presentation is atypical, there are no risk factors, and
there is a likely alternative diagnosis (e.g., angina, congestive heart failure). Many studies have
shown that the probability of pulmonary embolism in patients presenting with both low clinical probability (using either score) and normal D-dimer levels is so low that further imaging is
unnecessary and anticoagulation can safely be withheld.
Nonetheless, the D-dimer measurement is a nonspecific test, resulting in many false posi-
tives that prompt further diagnostic testing in low clinical probability patients. Such testing is
expensive, exposes patients to radiation, and could lead to overdiagnosis. In 2004, Kline proposed
the Pulmonary Embolism Rule-out Criteria (i.e., the “PERC” rule) to further identify patients at
such low risk of pulmonary embolism that no further testing (including D-dimer measurements)
is necessary.36 Importantly, to satisfy the rule, patients must be both low clinical probability (using
a structured rule [e.g., Tables 34.1 or 34.2] or gestalt) and must meet 8 objective criteria: (1) age
<50 years, (2) pulse <100 beats/min, (3) initial oxygen saturation >94% on room air, (4) no uni-
lateral leg swelling, (5) no hemoptysis, (6) no recent trauma or surgery, (7) no prior pulmonary
embolism or deep venous thrombosis, and (8) no exogenous estrogen use (patients meeting all
8 criteria are called “PERC negative”). If a patient is both low clinical probability and PERC
15,23,25,27,34,35
†
In these studies, the following risk factors and symptoms were found just as frequently in patients with
embolism as in those without it: female sex, older age, previous heart disease, previous lung disease, estrogen
use, recent trauma, dyspnea, chest pain (pleuritic or nonpleuritic), and cough. A few individual risk factors
have LRs between 1.4 and 2 and thus increase probability a small amount: cancer, recent immobilization,
recent surgery, and prior venous thromboembolism.
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