Acute Pleuritic Chest PainTim Baker

RURAL EMERGENCY MEDICINE

Centre for Rural Emergency MedicineSouth West Healthcare

Learning objectives

To recognise two common myths about pleuritic chest pain

To know when to order a D-dimer, CTPA, or V/Q scan

To know when to doubt the result of a CTPA

Outline

Pleuritic pain

Myths

Approach

Cases

What is pleuritic pain like?

Pain that is exacerbated during breathing, coughing, talking or sneezing

Breath holding relieves pain

Localised, shooting or stabbing

Can be constant background pain

Is it really pleuritic?

Poorly reliable - Kappa 0.4 (0.2 - 0.4 moderate agreement)

Pain on breathing versus hard to breath or pain on movement

Deep breath or cough only partially reproduces the pain

Pleuritic pain myths

Myth one: Pleuritic chest pain excludes acute coronary syndrome

pretest odds x likelihood ratio = post test odds

1 to 4 chance x 0.2 = 1 to 20 chance

Less likely, but not excluded

Precipitating and Aggravating FactorsAn easy-to-remember construct for pos-sible precipitating factors is the 3 p’s,which are chest pain that is pleuritic,positional, or reproducible with chestwall palpation.

Pleuritic Chest Pain. Chest pain thatis reproduced on deep inspiration orwith coughing is often associated withnon-ACS diseases such as pulmonaryembolism or costochondritis and hasbeen shown by several studies to be sug-gestive of non-AMI.2,3,25 In the study byLee et al,2 chest pain that was only par-tially pleuritic (deep breathing repro-duces the pain only sometimes) was aless valid discriminant than pain thatwas fully pleuritic.

Positional Chest Pain. Chest painthat is exacerbated by changes in posi-tion is thought to be more indicativeof nonischemic causes. For example,pericarditis is often alleviated by lean-ing forward, whereas musculoskeletalchest pain can typically be reproducedby arm or neck movement.32,41 Severalstudies have confirmed that a posi-tional component of chest pain repre-sents a non-ACS etiology.2,25

Palpable Chest Pain. Although chest-wall tenderness is technically part of thephysical examination, not the medicalhistory, several studies have demon-

strated that it suggests a non-ACS eti-ology.2,3,14,25

Exercise. The association betweenexercise and angina is well establishedin the literature.23,39,42 However, the re-lationship between exercise and AMI isless clearly elucidated. Mittleman et al43

established that, among AMI patients,heavy exertion in the hour precedingtheir event was common, confirming acorrelation between exercise and AMI.In addition, Goodacre et al14 found thatexertional pain is associated with AMI.Furthermore, when exertional pain islacking, the likelihood of AMI de-creases.

Emotion and Stress. Although sev-eral studies have suggested linkagesbetween emotional stress and AMI,attributing this relationship to highsympathetic activity, data to supportusing this as a discriminant to identifyACS have not been established.44-46 Ofnote, a syndrome of reversible cardio-myopathy triggered by emotionallystressful events and occurring primar-ily in women may mimic evolvingACS.47

Relieving Factors

Nitroglycerin. Previous thought heldthat rapid relief of chest pain with sub-lingual nitroglycerin strongly sup-

ports the diagnosis of angina.48,49 In ad-dition to relaxing coronary smoothmuscle, nitroglycerin causes relax-ation of esophageal muscle and thus canalleviate esophageal causes of chest painas well. Conventional teaching statesthat relief of cardiac pain is rapid (lessthan 5 minutes), whereas esophagealpain takes more than 10 minutes to sub-side.9 However, recent studies indi-cate that there is no association be-tween AMI and relief of chest pain withnitroglycerin.50,51

“GI Cocktail.” The GI cocktail iscommonly used in emergency depart-ments to treat dyspepsia. Composi-tions vary, but it is usually a mixtureof viscous lidocaine, a liquid antacid,and Donnatal (composed of several an-ticholinergics and a barbiturate). It hasbeen common practice to use the GIcocktail to differentiate cardiac fromesophageal chest pain according to astudy from the 1970s.52 However, morerecent studies and case series have con-tradicted these findings.53,54

Rest. Rest characteristically relievesthe pain associated with stable anginawithin 1 to 5 minutes.23 If pain con-tinues for longer than 10 minutesafter rest, the patient has traditionallybeen considered to be experiencingunstable angina, an AMI, or noncar-diac pain. In a comparison of cardiacand esophageal patients, 32 of 52(62%) with cardiac and 9 of 18 (50%)with esophageal pathology experi-enced relief of pain by rest (P=.39).9

This lack of significance from thissmall study makes it unclear whetherrelief of chest pain with rest is helpfulin differentiating ACS from noncar-diac pathology.

Associated SymptomsSeveral studies have examined the abil-ity of associated symptoms such as nau-sea, vomiting, and diaphoresis to pre-dict AMI.3,14,25-27 Two meta-analysesdiscovered that nausea and diaphoresispredict AMI.24,29 However, in the studyby Goodacre et al,14 the associationbetween nausea, vomiting, diaphoresis,and AMI disappeared on multivariabletesting.

Table 2. Value of Specific Components of the Chest Pain History for the Diagnosis of AcuteMyocardial Infarction (AMI)

Pain Descriptor Reference No. of PatientsPositive Likelihood

Ratio (95% CI)Increased likelihood of AMI

Radiation to right arm or shoulder 29 770 4.7 (1.9-12)Radiation to both arms or shoulders 14 893 4.1 (2.5-6.5)Associated with exertion 14 893 2.4 (1.5-3.8)Radiation to left arm 24 278 2.3 (1.7-3.1)Associated with diaphoresis 24 8426 2.0 (1.9-2.2)Associated with nausea or vomiting 24 970 1.9 (1.7-2.3)Worse than previous angina or similar

to previous MI29 7734 1.8 (1.6-2.0)

Described as pressure 29 11 504 1.3 (1.2-1.5)Decreased likelihood of AMI

Described as pleuritic 29 8822 0.2 (0.1-0.3)Described as positional 29 8330 0.3 (0.2-0.5)Described as sharp 29 1088 0.3 (0.2-0.5)Reproducible with palpation 29 8822 0.3 (0.2-0.4)Inframammary location 31 903 0.8 (0.7-0.9)Not associated with exertion 14 893 0.8 (0.6-0.9)

Abbreviations: AMI, acute myocardial infarction; CI, confidence interval.

CHEST PAIN HISTORY IN PATIENTS WITH SUSPECTED ACUTE CORONARY SYNDROMES

2626 JAMA, November 23/30, 2005—Vol 294, No. 20 (Reprinted) ©2005 American Medical Association. All rights reserved.

at MONASH MEDICAL CENTRE LIBRARY, on November 27, 2005 www.jama.comDownloaded from

Precipitating and Aggravating FactorsAn easy-to-remember construct for pos-sible precipitating factors is the 3 p’s,which are chest pain that is pleuritic,positional, or reproducible with chestwall palpation.

Pleuritic Chest Pain. Chest pain thatis reproduced on deep inspiration orwith coughing is often associated withnon-ACS diseases such as pulmonaryembolism or costochondritis and hasbeen shown by several studies to be sug-gestive of non-AMI.2,3,25 In the study byLee et al,2 chest pain that was only par-tially pleuritic (deep breathing repro-duces the pain only sometimes) was aless valid discriminant than pain thatwas fully pleuritic.

Positional Chest Pain. Chest painthat is exacerbated by changes in posi-tion is thought to be more indicativeof nonischemic causes. For example,pericarditis is often alleviated by lean-ing forward, whereas musculoskeletalchest pain can typically be reproducedby arm or neck movement.32,41 Severalstudies have confirmed that a posi-tional component of chest pain repre-sents a non-ACS etiology.2,25

Palpable Chest Pain. Although chest-wall tenderness is technically part of thephysical examination, not the medicalhistory, several studies have demon-

strated that it suggests a non-ACS eti-ology.2,3,14,25

Exercise. The association betweenexercise and angina is well establishedin the literature.23,39,42 However, the re-lationship between exercise and AMI isless clearly elucidated. Mittleman et al43

established that, among AMI patients,heavy exertion in the hour precedingtheir event was common, confirming acorrelation between exercise and AMI.In addition, Goodacre et al14 found thatexertional pain is associated with AMI.Furthermore, when exertional pain islacking, the likelihood of AMI de-creases.

Emotion and Stress. Although sev-eral studies have suggested linkagesbetween emotional stress and AMI,attributing this relationship to highsympathetic activity, data to supportusing this as a discriminant to identifyACS have not been established.44-46 Ofnote, a syndrome of reversible cardio-myopathy triggered by emotionallystressful events and occurring primar-ily in women may mimic evolvingACS.47

Relieving Factors

Nitroglycerin. Previous thought heldthat rapid relief of chest pain with sub-lingual nitroglycerin strongly sup-

ports the diagnosis of angina.48,49 In ad-dition to relaxing coronary smoothmuscle, nitroglycerin causes relax-ation of esophageal muscle and thus canalleviate esophageal causes of chest painas well. Conventional teaching statesthat relief of cardiac pain is rapid (lessthan 5 minutes), whereas esophagealpain takes more than 10 minutes to sub-side.9 However, recent studies indi-cate that there is no association be-tween AMI and relief of chest pain withnitroglycerin.50,51

“GI Cocktail.” The GI cocktail iscommonly used in emergency depart-ments to treat dyspepsia. Composi-tions vary, but it is usually a mixtureof viscous lidocaine, a liquid antacid,and Donnatal (composed of several an-ticholinergics and a barbiturate). It hasbeen common practice to use the GIcocktail to differentiate cardiac fromesophageal chest pain according to astudy from the 1970s.52 However, morerecent studies and case series have con-tradicted these findings.53,54

Rest. Rest characteristically relievesthe pain associated with stable anginawithin 1 to 5 minutes.23 If pain con-tinues for longer than 10 minutesafter rest, the patient has traditionallybeen considered to be experiencingunstable angina, an AMI, or noncar-diac pain. In a comparison of cardiacand esophageal patients, 32 of 52(62%) with cardiac and 9 of 18 (50%)with esophageal pathology experi-enced relief of pain by rest (P=.39).9

This lack of significance from thissmall study makes it unclear whetherrelief of chest pain with rest is helpfulin differentiating ACS from noncar-diac pathology.

Associated SymptomsSeveral studies have examined the abil-ity of associated symptoms such as nau-sea, vomiting, and diaphoresis to pre-dict AMI.3,14,25-27 Two meta-analysesdiscovered that nausea and diaphoresispredict AMI.24,29 However, in the studyby Goodacre et al,14 the associationbetween nausea, vomiting, diaphoresis,and AMI disappeared on multivariabletesting.

Table 2. Value of Specific Components of the Chest Pain History for the Diagnosis of AcuteMyocardial Infarction (AMI)

Pain Descriptor Reference No. of PatientsPositive Likelihood

Ratio (95% CI)Increased likelihood of AMI

Radiation to right arm or shoulder 29 770 4.7 (1.9-12)Radiation to both arms or shoulders 14 893 4.1 (2.5-6.5)Associated with exertion 14 893 2.4 (1.5-3.8)Radiation to left arm 24 278 2.3 (1.7-3.1)Associated with diaphoresis 24 8426 2.0 (1.9-2.2)Associated with nausea or vomiting 24 970 1.9 (1.7-2.3)Worse than previous angina or similar

to previous MI29 7734 1.8 (1.6-2.0)

Described as pressure 29 11 504 1.3 (1.2-1.5)Decreased likelihood of AMI

Described as pleuritic 29 8822 0.2 (0.1-0.3)Described as positional 29 8330 0.3 (0.2-0.5)Described as sharp 29 1088 0.3 (0.2-0.5)Reproducible with palpation 29 8822 0.3 (0.2-0.4)Inframammary location 31 903 0.8 (0.7-0.9)Not associated with exertion 14 893 0.8 (0.6-0.9)

Abbreviations: AMI, acute myocardial infarction; CI, confidence interval.

CHEST PAIN HISTORY IN PATIENTS WITH SUSPECTED ACUTE CORONARY SYNDROMES

2626 JAMA, November 23/30, 2005—Vol 294, No. 20 (Reprinted) ©2005 American Medical Association. All rights reserved.

at MONASH MEDICAL CENTRE LIBRARY, on November 27, 2005 www.jama.comDownloaded from

Precipitating and Aggravating FactorsAn easy-to-remember construct for pos-sible precipitating factors is the 3 p’s,which are chest pain that is pleuritic,positional, or reproducible with chestwall palpation.

Pleuritic Chest Pain. Chest pain thatis reproduced on deep inspiration orwith coughing is often associated withnon-ACS diseases such as pulmonaryembolism or costochondritis and hasbeen shown by several studies to be sug-gestive of non-AMI.2,3,25 In the study byLee et al,2 chest pain that was only par-tially pleuritic (deep breathing repro-duces the pain only sometimes) was aless valid discriminant than pain thatwas fully pleuritic.

Positional Chest Pain. Chest painthat is exacerbated by changes in posi-tion is thought to be more indicativeof nonischemic causes. For example,pericarditis is often alleviated by lean-ing forward, whereas musculoskeletalchest pain can typically be reproducedby arm or neck movement.32,41 Severalstudies have confirmed that a posi-tional component of chest pain repre-sents a non-ACS etiology.2,25

Palpable Chest Pain. Although chest-wall tenderness is technically part of thephysical examination, not the medicalhistory, several studies have demon-

strated that it suggests a non-ACS eti-ology.2,3,14,25

Exercise. The association betweenexercise and angina is well establishedin the literature.23,39,42 However, the re-lationship between exercise and AMI isless clearly elucidated. Mittleman et al43

established that, among AMI patients,heavy exertion in the hour precedingtheir event was common, confirming acorrelation between exercise and AMI.In addition, Goodacre et al14 found thatexertional pain is associated with AMI.Furthermore, when exertional pain islacking, the likelihood of AMI de-creases.

Emotion and Stress. Although sev-eral studies have suggested linkagesbetween emotional stress and AMI,attributing this relationship to highsympathetic activity, data to supportusing this as a discriminant to identifyACS have not been established.44-46 Ofnote, a syndrome of reversible cardio-myopathy triggered by emotionallystressful events and occurring primar-ily in women may mimic evolvingACS.47

Relieving Factors

Nitroglycerin. Previous thought heldthat rapid relief of chest pain with sub-lingual nitroglycerin strongly sup-

ports the diagnosis of angina.48,49 In ad-dition to relaxing coronary smoothmuscle, nitroglycerin causes relax-ation of esophageal muscle and thus canalleviate esophageal causes of chest painas well. Conventional teaching statesthat relief of cardiac pain is rapid (lessthan 5 minutes), whereas esophagealpain takes more than 10 minutes to sub-side.9 However, recent studies indi-cate that there is no association be-tween AMI and relief of chest pain withnitroglycerin.50,51

“GI Cocktail.” The GI cocktail iscommonly used in emergency depart-ments to treat dyspepsia. Composi-tions vary, but it is usually a mixtureof viscous lidocaine, a liquid antacid,and Donnatal (composed of several an-ticholinergics and a barbiturate). It hasbeen common practice to use the GIcocktail to differentiate cardiac fromesophageal chest pain according to astudy from the 1970s.52 However, morerecent studies and case series have con-tradicted these findings.53,54

Rest. Rest characteristically relievesthe pain associated with stable anginawithin 1 to 5 minutes.23 If pain con-tinues for longer than 10 minutesafter rest, the patient has traditionallybeen considered to be experiencingunstable angina, an AMI, or noncar-diac pain. In a comparison of cardiacand esophageal patients, 32 of 52(62%) with cardiac and 9 of 18 (50%)with esophageal pathology experi-enced relief of pain by rest (P=.39).9

This lack of significance from thissmall study makes it unclear whetherrelief of chest pain with rest is helpfulin differentiating ACS from noncar-diac pathology.

Associated SymptomsSeveral studies have examined the abil-ity of associated symptoms such as nau-sea, vomiting, and diaphoresis to pre-dict AMI.3,14,25-27 Two meta-analysesdiscovered that nausea and diaphoresispredict AMI.24,29 However, in the studyby Goodacre et al,14 the associationbetween nausea, vomiting, diaphoresis,and AMI disappeared on multivariabletesting.

Table 2. Value of Specific Components of the Chest Pain History for the Diagnosis of AcuteMyocardial Infarction (AMI)

Pain Descriptor Reference No. of PatientsPositive Likelihood

Ratio (95% CI)Increased likelihood of AMI

Radiation to right arm or shoulder 29 770 4.7 (1.9-12)Radiation to both arms or shoulders 14 893 4.1 (2.5-6.5)Associated with exertion 14 893 2.4 (1.5-3.8)Radiation to left arm 24 278 2.3 (1.7-3.1)Associated with diaphoresis 24 8426 2.0 (1.9-2.2)Associated with nausea or vomiting 24 970 1.9 (1.7-2.3)Worse than previous angina or similar

to previous MI29 7734 1.8 (1.6-2.0)

Described as pressure 29 11 504 1.3 (1.2-1.5)Decreased likelihood of AMI

Described as pleuritic 29 8822 0.2 (0.1-0.3)Described as positional 29 8330 0.3 (0.2-0.5)Described as sharp 29 1088 0.3 (0.2-0.5)Reproducible with palpation 29 8822 0.3 (0.2-0.4)Inframammary location 31 903 0.8 (0.7-0.9)Not associated with exertion 14 893 0.8 (0.6-0.9)

Abbreviations: AMI, acute myocardial infarction; CI, confidence interval.

CHEST PAIN HISTORY IN PATIENTS WITH SUSPECTED ACUTE CORONARY SYNDROMES

2626 JAMA, November 23/30, 2005—Vol 294, No. 20 (Reprinted) ©2005 American Medical Association. All rights reserved.

at MONASH MEDICAL CENTRE LIBRARY, on November 27, 2005 www.jama.comDownloaded from

Precipitating and Aggravating FactorsAn easy-to-remember construct for pos-sible precipitating factors is the 3 p’s,which are chest pain that is pleuritic,positional, or reproducible with chestwall palpation.

Pleuritic Chest Pain. Chest pain thatis reproduced on deep inspiration orwith coughing is often associated withnon-ACS diseases such as pulmonaryembolism or costochondritis and hasbeen shown by several studies to be sug-gestive of non-AMI.2,3,25 In the study byLee et al,2 chest pain that was only par-tially pleuritic (deep breathing repro-duces the pain only sometimes) was aless valid discriminant than pain thatwas fully pleuritic.

Positional Chest Pain. Chest painthat is exacerbated by changes in posi-tion is thought to be more indicativeof nonischemic causes. For example,pericarditis is often alleviated by lean-ing forward, whereas musculoskeletalchest pain can typically be reproducedby arm or neck movement.32,41 Severalstudies have confirmed that a posi-tional component of chest pain repre-sents a non-ACS etiology.2,25

Palpable Chest Pain. Although chest-wall tenderness is technically part of thephysical examination, not the medicalhistory, several studies have demon-

strated that it suggests a non-ACS eti-ology.2,3,14,25

Exercise. The association betweenexercise and angina is well establishedin the literature.23,39,42 However, the re-lationship between exercise and AMI isless clearly elucidated. Mittleman et al43

established that, among AMI patients,heavy exertion in the hour precedingtheir event was common, confirming acorrelation between exercise and AMI.In addition, Goodacre et al14 found thatexertional pain is associated with AMI.Furthermore, when exertional pain islacking, the likelihood of AMI de-creases.

Emotion and Stress. Although sev-eral studies have suggested linkagesbetween emotional stress and AMI,attributing this relationship to highsympathetic activity, data to supportusing this as a discriminant to identifyACS have not been established.44-46 Ofnote, a syndrome of reversible cardio-myopathy triggered by emotionallystressful events and occurring primar-ily in women may mimic evolvingACS.47

Relieving Factors

Nitroglycerin. Previous thought heldthat rapid relief of chest pain with sub-lingual nitroglycerin strongly sup-

ports the diagnosis of angina.48,49 In ad-dition to relaxing coronary smoothmuscle, nitroglycerin causes relax-ation of esophageal muscle and thus canalleviate esophageal causes of chest painas well. Conventional teaching statesthat relief of cardiac pain is rapid (lessthan 5 minutes), whereas esophagealpain takes more than 10 minutes to sub-side.9 However, recent studies indi-cate that there is no association be-tween AMI and relief of chest pain withnitroglycerin.50,51

“GI Cocktail.” The GI cocktail iscommonly used in emergency depart-ments to treat dyspepsia. Composi-tions vary, but it is usually a mixtureof viscous lidocaine, a liquid antacid,and Donnatal (composed of several an-ticholinergics and a barbiturate). It hasbeen common practice to use the GIcocktail to differentiate cardiac fromesophageal chest pain according to astudy from the 1970s.52 However, morerecent studies and case series have con-tradicted these findings.53,54

Rest. Rest characteristically relievesthe pain associated with stable anginawithin 1 to 5 minutes.23 If pain con-tinues for longer than 10 minutesafter rest, the patient has traditionallybeen considered to be experiencingunstable angina, an AMI, or noncar-diac pain. In a comparison of cardiacand esophageal patients, 32 of 52(62%) with cardiac and 9 of 18 (50%)with esophageal pathology experi-enced relief of pain by rest (P=.39).9

This lack of significance from thissmall study makes it unclear whetherrelief of chest pain with rest is helpfulin differentiating ACS from noncar-diac pathology.

Associated SymptomsSeveral studies have examined the abil-ity of associated symptoms such as nau-sea, vomiting, and diaphoresis to pre-dict AMI.3,14,25-27 Two meta-analysesdiscovered that nausea and diaphoresispredict AMI.24,29 However, in the studyby Goodacre et al,14 the associationbetween nausea, vomiting, diaphoresis,and AMI disappeared on multivariabletesting.

Table 2. Value of Specific Components of the Chest Pain History for the Diagnosis of AcuteMyocardial Infarction (AMI)

Pain Descriptor Reference No. of PatientsPositive Likelihood

Ratio (95% CI)Increased likelihood of AMI

Radiation to right arm or shoulder 29 770 4.7 (1.9-12)Radiation to both arms or shoulders 14 893 4.1 (2.5-6.5)Associated with exertion 14 893 2.4 (1.5-3.8)Radiation to left arm 24 278 2.3 (1.7-3.1)Associated with diaphoresis 24 8426 2.0 (1.9-2.2)Associated with nausea or vomiting 24 970 1.9 (1.7-2.3)Worse than previous angina or similar

to previous MI29 7734 1.8 (1.6-2.0)

Described as pressure 29 11 504 1.3 (1.2-1.5)Decreased likelihood of AMI

Described as pleuritic 29 8822 0.2 (0.1-0.3)Described as positional 29 8330 0.3 (0.2-0.5)Described as sharp 29 1088 0.3 (0.2-0.5)Reproducible with palpation 29 8822 0.3 (0.2-0.4)Inframammary location 31 903 0.8 (0.7-0.9)Not associated with exertion 14 893 0.8 (0.6-0.9)

Abbreviations: AMI, acute myocardial infarction; CI, confidence interval.

CHEST PAIN HISTORY IN PATIENTS WITH SUSPECTED ACUTE CORONARY SYNDROMES

2626 JAMA, November 23/30, 2005—Vol 294, No. 20 (Reprinted) ©2005 American Medical Association. All rights reserved.

at MONASH MEDICAL CENTRE LIBRARY, on November 27, 2005 www.jama.comDownloaded from

Chance of Acute Myocardial Infarction

Swap, 2005, JAMA, 294(20):2623-9.

(20 %) (5 %)

Pleuritic chest is unhelpful if

There are other findings or risk factors that suggest a cardiac cause

You are looking for unstable angina, not AMI

Pain is only partially reproducible

Myth two: Pleuritic pain ≡ Pulmonary embolus

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Poor sensitivity

Only 50 % of PE patients have pain

Poor specificity

Chest pain - 1 % has a pulmonary embolus

Pleuritic chest pain - 5 % has a pulmonary embolus

Frequency doubles each with decade of life

We often worry in the young and fit, but should mainly worry in the old and unwell

Approach

History, examination, O2 saturation , ECG

EffusionInfiltrate

Investigateand treatObvious cause

Separation

Chest x-ray

CardiomegalyClear

PneumothoraxPneumonia,malignancy,

pulmonary embolus ACS work up

Could this bea pulmonary

embolus?

Could this beacute coronary

syndrome?

Transudate,pus,

tumour,blood

Chronicpericarditis

Pleuritic chest pain

PE work up

Undifferentiated chest pain

Cases

Case one - Mrs Gladys Notme

A 71-year-old woman presents with one day pleuritic left posterior chest pain and shortnesss of breath. She was in hospital three weeks ago with an exacerbation of COPD. She has diabetes, hypertension, and had a DVT 10 years ago. Her temperature is 37.2°C, and her pulse is 105 beats per minute. Physical examination discloses occasional wheeze, but is otherwise unremarkable. An electrocardiogram and chest radiograph are both normal.

Would a D-dimer be useful?

How useful is a D-dimer?

False positive = 48 % Positive likelihood ratio = 2

Negative likelihood ratio = 0.07LR- 0.07

1 % chance of PE

10 % chance of PE

10 %

60 %

Low risk

High risk

Low clinical risk

Chance of PE(after history and exam)

10 %

Chance of PE 20 %

Chance of PE 1 %NegativeD-Dimer

PositiveD-Dimer

LR- 0.07LR+ 2.0

High clinical risk

Chance of PE(after history and exam)

60 %

Chance of PE 75 %

Chance of PE 10 %NegativeD-Dimer

PositiveD-Dimer

LR- 0.07LR+ 2.0

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Strategies for Ruling Out PE in the ED %&'()&"*"+,-*,&./"0*+&1"2)"/23-"4*,(&),"42435*,(2)6"*7*(5*05&"-&+23-8&+6"*)1"4-*8,(8&"+&,,().9"":++&++",;&"4*,(&),<+")&&1"'2-",&+,().6"*)1"4-&!,&+,"5(=&5(;221"2'">?"3+().",;&"85()(8*5".3(1&+"1&+8-(0&1"*027&"@>?AB6"C&55+6"D&)&7*6"2-"/23-"E2+,"5(=&5/"1(*.)2+(+F9"G;&)"3,(5(H&"%!1(E&-+"()"52I"-(+="4*,(&),+",2"&J8531&"7&)23+",;-2E02&E025(+E9"K,&()"*)1",;&">LM>?%"LL"()7&+,(.*,2-+"*,,&E4,&1",2"-&82)8(5&",;&"'()1().+"()",;&(-"()7&+,(.*,(2)"*)1",;2+&"2'",;&"B;-(+,24;&-"D-234"*)1"4-&+&),&1",;&"'2552I()."-&82EE&)1&1"1(*.)2+,(8"4*,;I*/+9N$OP"""

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When is a D-dimer useful?

What is the clinical risk?

C L I N I C A L P O L I C Y

Exclusion criteria. Pregnant patients and asymptomaticpatients.

C R I T I C A L I S S U E S I N P U L M O N A R YE M B O L I S M

Estimation of pretest probability of the disease is imper-ative for proper application of results of diagnostic test-ing. The pretest probability of PE can be estimated byusing explicit criteria that are available in virtuallyevery ED. Multiple methods have been examined, butthe 3 methods that appear to be most applicable to EDpatients are the Wells et al39-41 criteria derived from athromboembolism referral center in Canada, the Wickiet al42 criteria derived from a single hospital in Switzer-land, and the Kline et al43 criteria derived from 7 urbanEDs in the United States. The Wells et al and Wicki et alscoring system assign a number to certain specific find-ings in patients with suspected PE (Table 1 and 2). Thenumbers are added up to generate a score, which corre-sponds to a pretest probability for PE. With either sys-tem, low-risk patients (40% to 49% of total patients)had less than a 10% probability of PE, and high-riskpatients (6% to 7% of total patients) had greater than

2 6 0 A N N A L S O F E M E R G E N C Y M E D I C I N E 4 1 : 2 F E B R U A R Y 2 0 0 3

65% probability of PE. Intermediate-risk patients com-prised approximately half of the patients with a proba-bility of PE in the 20% to 40% range. Sanson et al44 per-formed a multicenter trial comparing subjectivephysician judgement of pretest probability for PE to theextended Wells et al39 model and the simplified Wells etal40,41 model. In this study, the rates of PE in the low-risk groups were 19% for subjective physician judge-ment, 28% for the extended Wells et al model, and 28%in the simplified Wells et al44 model. The 3 methodsyielded comparative predictive values in patients withintermediate and high risk for PE. These findingsemphasize the need for ongoing prospective studies tovalidate and improve structured models for predictingrisk of PE.45 The Kline et al43 scoring system was devel-oped to identify patients who were safe for use of D-dimertesting for exclusion of PE (Figure). In this study, 934patients with suspected PE were prospectively inter-

Table 1.Wells et al41 criteria for assessment of pretest probability forPE.

Criteria Points

Suspected DVT 3.0An alternative diagnosis is less likely than PE 3.0Heart rate >100 beats/min 1.5Immobilization or surgery in the previous 4 wk 1.5Previous DVT/PE 1.5Hemoptysis 1.0Malignancy (on treatment, treated in the past 6 mo or palliative) 1.0

Mean Probability % With InterpretationScore Range of PE, % This Score of Risk

<2 points 3.6 40 Low2–6 points 20.5 53 Moderate>6 points 66.7 7 High

Reprinted with permission from Wells PS, Anderson DR, Rodger M, et al. Derivation ofa simple clinical model to categorize patient’s probability of pulmonary embolism:increasing the models utility with the SimpliRED D-dimer. Thromb Haemost.2000;83:416-420.

Table 2.Wicki et al42 criteria for assessment of pretest probability forPE.

Criteria Points

Age 60–79, y 1Age >79, y 2Prior DVT/PE 2Recent surgery 3Heart rate >100 beats/min 1PaCO2, mm Hg<36 236–39 1PaO2, mm Hg<49 449–60 3>60–71 2>71–82 1Chest x-rayPlate-like atelectasis 1Elevation of hemidiaphragm 1

Mean Probability % With InterpretationScore Range of PE, % This Score of Risk

0–4 10 49 Low5–8 38 44 Moderate9–12 81 6 High

Reprinted with permission from Wicki J, Perneger T, Junod A, et al. Assessing clinicalprobability of pulmonary embolism in the emergency ward: a simple score. Arch InternMed. 2001;161:92-97. Copyrighted 2001, American Medical Association.

Well’s criteria

Case one - Mrs Gladys NotmeA 71-year-old woman presents with one day pleuritic left posterior chest pain, and shortnesss of breath. She was in hospital three weeks ago (1.5) with an exacerbation of COPD. She has diabetes, hypertension, and had a DVT (1.5) 10 years ago. Her temperature is 37.2°C, and her pulse is 105 beats per minute (1.5). Physical examination discloses occasional wheeze, but is otherwise unremarkable. An electrocardiogram and chest radiograph are both normal (3).

C L I N I C A L P O L I C Y

Exclusion criteria. Pregnant patients and asymptomaticpatients.

C R I T I C A L I S S U E S I N P U L M O N A R YE M B O L I S M

Estimation of pretest probability of the disease is imper-ative for proper application of results of diagnostic test-ing. The pretest probability of PE can be estimated byusing explicit criteria that are available in virtuallyevery ED. Multiple methods have been examined, butthe 3 methods that appear to be most applicable to EDpatients are the Wells et al39-41 criteria derived from athromboembolism referral center in Canada, the Wickiet al42 criteria derived from a single hospital in Switzer-land, and the Kline et al43 criteria derived from 7 urbanEDs in the United States. The Wells et al and Wicki et alscoring system assign a number to certain specific find-ings in patients with suspected PE (Table 1 and 2). Thenumbers are added up to generate a score, which corre-sponds to a pretest probability for PE. With either sys-tem, low-risk patients (40% to 49% of total patients)had less than a 10% probability of PE, and high-riskpatients (6% to 7% of total patients) had greater than

2 6 0 A N N A L S O F E M E R G E N C Y M E D I C I N E 4 1 : 2 F E B R U A R Y 2 0 0 3

65% probability of PE. Intermediate-risk patients com-prised approximately half of the patients with a proba-bility of PE in the 20% to 40% range. Sanson et al44 per-formed a multicenter trial comparing subjectivephysician judgement of pretest probability for PE to theextended Wells et al39 model and the simplified Wells etal40,41 model. In this study, the rates of PE in the low-risk groups were 19% for subjective physician judge-ment, 28% for the extended Wells et al model, and 28%in the simplified Wells et al44 model. The 3 methodsyielded comparative predictive values in patients withintermediate and high risk for PE. These findingsemphasize the need for ongoing prospective studies tovalidate and improve structured models for predictingrisk of PE.45 The Kline et al43 scoring system was devel-oped to identify patients who were safe for use of D-dimertesting for exclusion of PE (Figure). In this study, 934patients with suspected PE were prospectively inter-

Table 1.Wells et al41 criteria for assessment of pretest probability forPE.

Criteria Points

Suspected DVT 3.0An alternative diagnosis is less likely than PE 3.0Heart rate >100 beats/min 1.5Immobilization or surgery in the previous 4 wk 1.5Previous DVT/PE 1.5Hemoptysis 1.0Malignancy (on treatment, treated in the past 6 mo or palliative) 1.0

Mean Probability % With InterpretationScore Range of PE, % This Score of Risk

<2 points 3.6 40 Low2–6 points 20.5 53 Moderate>6 points 66.7 7 High

Reprinted with permission from Wells PS, Anderson DR, Rodger M, et al. Derivation ofa simple clinical model to categorize patient’s probability of pulmonary embolism:increasing the models utility with the SimpliRED D-dimer. Thromb Haemost.2000;83:416-420.

Table 2.Wicki et al42 criteria for assessment of pretest probability forPE.

Criteria Points

Age 60–79, y 1Age >79, y 2Prior DVT/PE 2Recent surgery 3Heart rate >100 beats/min 1PaCO2, mm Hg<36 236–39 1PaO2, mm Hg<49 449–60 3>60–71 2>71–82 1Chest x-rayPlate-like atelectasis 1Elevation of hemidiaphragm 1

Mean Probability % With InterpretationScore Range of PE, % This Score of Risk

0–4 10 49 Low5–8 38 44 Moderate9–12 81 6 High

Reprinted with permission from Wicki J, Perneger T, Junod A, et al. Assessing clinicalprobability of pulmonary embolism in the emergency ward: a simple score. Arch InternMed. 2001;161:92-97. Copyrighted 2001, American Medical Association.

Score = 7.5High risk

High risk imaging

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CT pulmonary angiography

Repeat CTPA if poor quality, add CT venography,ultrasound, V/Q, MRI, or ultrasound

CTPA negative (NPV 60 %) CTPA positive (PPV 96 %)✰

Case two - Mr Justin Case

A 66-year-old man presents with two days of dry cough and pleuritic right sided chest pain, one week after a flight from Peru. He is otherwise well, with no relevant past illness. His temperature is 37.2°C, and his pulse is 80 beats per minute. Physical examination, electrocardiogram and chest radiograph are all normal.

What is your approach?

Case two - Mr Justin Case

A 66-year-old man presents with two days of dry cough and pleuritic right sided chest pain, one week after a flight from Mexico (1.5). He is otherwise well, with no relevant past illness. His temperature is 37.2°C, and his pulse is 80 beats per minute. Physical examination, electrocardiogram and chest radiograph are all normal.

C L I N I C A L P O L I C Y

Exclusion criteria. Pregnant patients and asymptomaticpatients.

C R I T I C A L I S S U E S I N P U L M O N A R YE M B O L I S M

Estimation of pretest probability of the disease is imper-ative for proper application of results of diagnostic test-ing. The pretest probability of PE can be estimated byusing explicit criteria that are available in virtuallyevery ED. Multiple methods have been examined, butthe 3 methods that appear to be most applicable to EDpatients are the Wells et al39-41 criteria derived from athromboembolism referral center in Canada, the Wickiet al42 criteria derived from a single hospital in Switzer-land, and the Kline et al43 criteria derived from 7 urbanEDs in the United States. The Wells et al and Wicki et alscoring system assign a number to certain specific find-ings in patients with suspected PE (Table 1 and 2). Thenumbers are added up to generate a score, which corre-sponds to a pretest probability for PE. With either sys-tem, low-risk patients (40% to 49% of total patients)had less than a 10% probability of PE, and high-riskpatients (6% to 7% of total patients) had greater than

2 6 0 A N N A L S O F E M E R G E N C Y M E D I C I N E 4 1 : 2 F E B R U A R Y 2 0 0 3

65% probability of PE. Intermediate-risk patients com-prised approximately half of the patients with a proba-bility of PE in the 20% to 40% range. Sanson et al44 per-formed a multicenter trial comparing subjectivephysician judgement of pretest probability for PE to theextended Wells et al39 model and the simplified Wells etal40,41 model. In this study, the rates of PE in the low-risk groups were 19% for subjective physician judge-ment, 28% for the extended Wells et al model, and 28%in the simplified Wells et al44 model. The 3 methodsyielded comparative predictive values in patients withintermediate and high risk for PE. These findingsemphasize the need for ongoing prospective studies tovalidate and improve structured models for predictingrisk of PE.45 The Kline et al43 scoring system was devel-oped to identify patients who were safe for use of D-dimertesting for exclusion of PE (Figure). In this study, 934patients with suspected PE were prospectively inter-

Table 1.Wells et al41 criteria for assessment of pretest probability forPE.

Criteria Points

Suspected DVT 3.0An alternative diagnosis is less likely than PE 3.0Heart rate >100 beats/min 1.5Immobilization or surgery in the previous 4 wk 1.5Previous DVT/PE 1.5Hemoptysis 1.0Malignancy (on treatment, treated in the past 6 mo or palliative) 1.0

Mean Probability % With InterpretationScore Range of PE, % This Score of Risk

<2 points 3.6 40 Low2–6 points 20.5 53 Moderate>6 points 66.7 7 High

Reprinted with permission from Wells PS, Anderson DR, Rodger M, et al. Derivation ofa simple clinical model to categorize patient’s probability of pulmonary embolism:increasing the models utility with the SimpliRED D-dimer. Thromb Haemost.2000;83:416-420.

Table 2.Wicki et al42 criteria for assessment of pretest probability forPE.

Criteria Points

Age 60–79, y 1Age >79, y 2Prior DVT/PE 2Recent surgery 3Heart rate >100 beats/min 1PaCO2, mm Hg<36 236–39 1PaO2, mm Hg<49 449–60 3>60–71 2>71–82 1Chest x-rayPlate-like atelectasis 1Elevation of hemidiaphragm 1

Mean Probability % With InterpretationScore Range of PE, % This Score of Risk

0–4 10 49 Low5–8 38 44 Moderate9–12 81 6 High

Reprinted with permission from Wicki J, Perneger T, Junod A, et al. Assessing clinicalprobability of pulmonary embolism in the emergency ward: a simple score. Arch InternMed. 2001;161:92-97. Copyrighted 2001, American Medical Association.

Score = 1.5Low risk

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Rule out pulmonary embolism

Low risk imaging

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CT pulmonary angiography

CTPA negative (NPV 96 %) CTPA positive (PPV 58 %)

Repeat CTPA if poor quality, add CT venography,ultrasound, V/Q, MRI, or ultrasound

✰

Intermediate risk imaging

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CT pulmonary angiography

CTPA negative (NPV 89 %) CTPA positive (PPV 92 %)

Add CT venography,ultrasound, V/Q, MRI, or ultrasound

✰

Case three - Mr Knut Tuscick

A 34-year-old man woke today with pleuritic right sided chest pain, partially relieved with neurofen. He has no associated symptoms. He is otherwise well, but not very fit. The tree planting he attended yesterday was his first really hard physical exertion for months. He has no relevant past illness and takes no medications. His temperature is 36°C, and his pulse is 80 beats per minute. Physical examination, electrocardiogram and chest radiograph are all normal.

What is your approach?

“No risk” of pulmonary embolism

Pulmonary EmbolismRule-out Criteria (PERC)

Likelihood ratio of 0.17

No fatal PE in 1500 patients

PERC(Workup if any one abnormal)

Age < 50Pulse <100

Oxygen saturation > 94%No unilateral leg swelling

No haemoptysisNo recent surgery or trauma

No prior PE or DVTNo hormone use

Case four - Ms Sophia Choice

A 28-year-old woman who is 32 weeks pregnant presents with three days of severe pleuritic left chest pain and shortnesss of breath. The pregnancy has been unremarkable, and she has no relevant past illnesses. Her temperature is 37.2°C, and her pulse is 105 beats per minute. An electrocardiogram and chest radiograph are both normal. D-dimer is positive and lower limb doppler is negative.

What is your approach

V/Q or CTPA?V / Q scan

1 mSv radiation

99mTc albumin 0.9 mSv

133Xe <0.01 mSv

Radiation reaches foetus in blood and from bladder

Indeterminate scans common (but less so in the young)

CTPA

14 mSv radiation to mother

Only 1 % scatters to embryo

0.14 mSv to foetus (T3)

Risks of radiationFor foetus

Increased risk of childhood cancer

V/Q by 1 in 280,000

CTPA by 1 in 1,000,000

(100 mSv needed for CNS malformations)

For mother

Increased risk of breast cancer

V/Q - practically no increase

CTPA 1 in 2000

From a background risk of 10 in 2000 to 11 in 2000

Conclusion

SummaryPleuritic chest pain excludes acute coronary syndrome

Pleuritic chest pain ≡ pulmonary embolus

D-Dimer should be used in low and intermediate risk patients (not “no risk” or high risk patients)

negative excludes PE

positive requires further testing

Consider further testing when CTPA disagrees with clinical picture

Inform pregnant patients of radiation risks

Questions?

ReferencesSwap, CJ.J. Nagurney, J.T. 2005, Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes, JAMA. Nov 23;294(20):2623-9.

Bowman, s. h. (2007, October 8). The ever elusive pulmonary embolism: A logical approach. ACEP scientific assembly. http://www.acep.org/WorkArea/DownloadAsset.aspx?id=46350

American College of Emergency Physicians Clinical Policies Committee & Clinical Policies Committee Subcommittee on Suspected Pulmonary Embolism, 2003, Clinical policy: critical issues in the evaluation and management of adult patients presenting with suspected pulmonary embolism, Annals of emergency medicine, 41(2), pp. 257-70.

Tapson, V.F., 2008, Acute pulmonary embolism, The New England journal of medicine, 358(10), pp. 1037-52.

Kline, J. A., Mitchell, A. M., Kabrhel, C., Richman, P. B., & Courtney, D. M. (2004). Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost, 2(8), 1247-55.

Marik, P.E. & Plante, L.A., 2008, Venous thromboembolic disease and pregnancy, The New England journal of medicine, 359(19), pp. 2025-33.