Original Article

Prevalence and predictors of pulmonary embolism in

patients with acute exacerbation of chronic obstructive
pulmonary disease
Nasir Chaudhary1, Umar Hafiz Khan2, Tajamul Hussain Shah3, Feroze Shaheen4, Suhail Mantoo5,
Syed Mudasir Qadri5, Nazia Mehfooz3, Afshan Shabir2, Farhana Siraj5, Sonaullah Shah6, Parvaiz A Koul6,
Rafi Ahmed Jan6
1
Department of Cardiology, GMC, Jammu, Jammu and Kashmir, India, 2Department of Geriatric Medicine, Sher E Kashmir Institute
of Medical Sciences, Srinagar, Jammu and Kashmir, India, 3Department of Pulmonary Medicine, Sher E Kashmir Institute of Medical
Sciences, Srinagar, Jammu and Kashmir, India, 4Department of Radiology, Sher E Kashmir Institute of Medical Sciences, Srinagar, Jammu
and Kashmir, India, 5Department of Internal Medicine, Sher E Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India,
6
Department of Internal and Pulmonary Medicine, Sher E Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

ABSTRACT

Background: The prevalence of pulmonary embolism (PE) in patients of acute exacerbation of chronic obstructive
pulmonary disease (AECOPD) varies over a wide range. Early detection and treatment of PE in AECOPD is a key to
improve patient outcome. The purpose of the study was to investigate the prevalence and predictors of PE in patients
of AECOPD in a high burden region of North India. Materials and Methods: This prospective study included patients
of AECOPD with no obvious cause of exacerbation on initial evaluation. Apart from routine workup, the participants
underwent assessment of D‑dimer, compression ultrasound and venous Doppler ultrasound of the lower limbs and pelvic
veins, and a multidetector computed tomography pulmonary angiography. Results: A total of 100 patients of AECOPD
with unknown etiology were included. PE as a possible cause of AE‑COPD was observed in 14% of patients. Among the
participants with PE, 63% (n = 9) had a concomitant presence of lower extremity deep venous thrombosis. Hemoptysis
and chest pain were significantly higher in patients of AECOPD with PE ([35.7% vs. 7%, P = 0.002] and [92.9% vs. 38.4%,
P = 0.001]). Likelihood of PE was significantly higher in patients who presented with tachycardia, tachypnea, respiratory
alkalosis (PaCO2 <45 mmHg and pH >7.45), and hypotension. No difference was observed between the two groups
in terms of in‑hospital mortality, age, sex distribution, and risk factors for embolism except for the previous history of
venous thromboembolism (35.7% vs. 12.8% P = 0.03). Conclusion: PE was probably responsible for AECOPD in 14%
of patients with no obvious cause on initial assessment. Patients who present with chest pain, hemoptysis, tachypnea,
tachycardia, and respiratory alkalosis should be particularly screened for PE.

KEY WORDS: Acute exacerbation, chronic obstructive pulmonary disease, D‑dimer, pulmonary embolism

Address for correspondence: Prof. Rafi Ahmed Jan, Department of Internal and Pulmonary Medicine, Sher E Kashmir Institute of Medical Sciences, Soura,
Srinagar ‑ 190 011, Jammu and Kashmir, India. E‑mail: rafiahmedjan@gmail.com

Submitted: 03-Feb-2020 Revised: 12-Jun-2021 Accepted: 15-Jul-2021 Published: 26-Oct-2021

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How to cite this article: Chaudhary N, Khan UH, Shah TH,

DOI: Shaheen F, Mantoo S, Qadri SM, et al. Prevalence and predictors of
pulmonary embolism in patients with acute exacerbation of chronic
10.4103/lungindia.lungindia_79_21 obstructive pulmonary disease. Lung India 2021;38:533-9.

© 2021 Indian Chest Society | Published by Wolters Kluwer - Medknow 533

 Chaudhary, et al.: Prevalence and predictors of PE in patients with AECOPD

INTRODUCTION Study population

Patients of COPD who presented with AE‑COPD to the
Chronic obstructive pulmonary disease (COPD) is currently emergency department of our institute severe enough to
the 4th leading cause of death worldwide and 2nd in India.[1] require hospitalization were assessed for the eligibility
Patients with COPD may present with acute worsening of criteria. Patients of AECOPD with no obvious cause on
their respiratory symptoms known as acute exacerbation initial assessment were included in the study. Following
of chronic obstructive pulmonary disease (AECOPD).[2] In assessments were done to rule out the possible etiology
addition to increased morbidity and health‑care utilization, of worsening of symptoms in patients with COPD: (a)
AE‑COPD significantly reduces both in‑hospital and history of fever, purulent sputum, myalgias, and running
long‑term survival.[3‑5] Majority (50%–70%) of the events nose to rule out possibility of infective etiology; (b)
of AECOPD are precipitated by respiratory tract infections, chest radiography was done to look for the evidence
followed by exposure to environmental pollution (10%). of pneumothorax, pleural effusion, or pulmonary
However, in up to 30% of cases, the cause of exacerbation edema as a cause of exacerbation of symptoms. (c)
remains unknown.[6,7] Electrocardiography to look for any evidence suggestive
of acute coronary syndrome and arrhythmias. Those with
Various studies have reported COPD as one of the independent definite alternative cause of worsening of symptoms (like
risk factors for venous thromboembolism (VTE). [8,9] respiratory tract infection, pneumothorax, and myocardial
In a systematic review and meta‑analysis, the pooled ischemia) plus requiring mechanical ventilation or
prevalence of pulmonary embolism (PE) in unexplained who fail to give consent were excluded from the study.
AECOPD was reported to be 16.1%. [10] In a recent Diagnosis of COPD was made based on the compatible
multicenter cross‑sectional study (n = 740), the prevalence history and postbronchodilator forced expiratory volume
of PE was 5.9% (11% in patients with suspicion of PE in 1 s to forced vital capacity ratio of <0.7. Severity of
and 4.3% in patients with no suspicion of PE on initial COPD as well as exacerbation of COPD was defined as
per the global initiative for chronic obstructive lung
assessment).[11] However, higher prevalence of PE was
disease (GOLD) criteria.[20]
reported in postmortem studies ranging from 28% to
51%.[12,13] In addition, patients of COPD with PE have
Study protocol
significantly higher 3 month as well as 1 year mortality
In addition to routine investigations that included
compared to patients with PE alone.[14,15] It is therefore
complete blood count, biochemistry, chest radiograph,
important to identify PE as a cause of AECOPD, as
and arterial blood gas (ABG) analysis, a detailed history,
delay in diagnosis and treatment is associated with
physical examination, the use of pretest probability
poorer outcome.[16] As the symptoms of AECOPD are
scoring (simplified Geneva scoring [SGS]), and qualitative
nonspecific, it is often difficult to differentiate PE as a
D‑dimer assay were carried out in all the participants.
cause of AECOPD based on clinical examination alone.
Compression ultrasound (CUS) and venous Doppler of
Multidetector computed tomography (MDCT) pulmonary
lower extremities were performed for the presence of deep
angiography (PA) is currently the investigation of choice
venous thrombosis (DVT) followed by MDCT PA for PE.
in suspected PE.[17]
Reporting of CUS/Doppler study of lower extremities and
MDCT‑PA was done by a radiologist with more than 10‑year
The reported prevalence of spirometrically defined experience in a teaching tertiary care center [Figure 1].
COPD (in adults ≥ 40 years) in our part of world is 17.3%
in males and 14.8% in females.[18] It is higher than that Diagnosis of deep venous thrombosis and pulmonary
reported from other states of our country and various embolism
parts of the world.[19] We have previously reported that Noncompressibility or incomplete compressibility of deep
viral respiratory tract infections are responsible for acute veins of lower extremities on CUS was taken as criteria for
exacerbation in sizable number of our COPD patients.[7] the presence of DVT. Computed tomography pulmonary
However, the cause of AECOPD remains unknown in angiogram (CTPA) was considered positive for PE if there
a large number of patients. With this background, the was a total occlusion of the vessel by a low attenuation
present study was designed to know the prevalence of PE material or presence of an intraluminal defect surrounded
in patients with AECOPD with no identifiable etiology by a contrast material.[21] Patients were considered to have
requiring hospitalization at a tertiary care hospital of PE if they had positive CTPA or positive CUS/Doppler of
Kashmir in North India. lower extremities plus high clinical suspicion (if CTPA
was not done due to any contraindication). PE was
MATERIALS AND METHODS excluded in case of negative CTPA and/or lower extremity
CUS/Doppler. History regarding the presence of risk factors
Study design and place for VTE including the presence of malignancy, immobility,
This study was a prospective observational study that recent surgery, or previous VTE was recorded. Patients
was conducted over a period of 2 years in Sheri‑Kashmir who had DVT or PTE were managed with therapeutic
institute of medical sciences, a multidisplinary institute anticoagulation and those with PE who fulfilled the criteria
of north India, an 800‑bedded hospital. for thrombolysis, received thrombolysis as per the standard

534 Lung India • Volume 38 • Issue 6 • November-December 2021

 Chaudhary, et al.: Prevalence and predictors of PE in patients with AECOPD

Patients with AE-COPD in main pulmonary artery, followed by segmental (38.5%)

presenting to AE and at subsegmental (15%) level [Table 2]. None of the cases
Evaluated for Cause
of AECOPD with negative CTPA had DVT on CUS/Doppler lower limbs.
No significant difference was observed between severity of
(n = 100) patients of AECOPD with AECOPD and presence of PE (P = 0.521) [Table 1].
no Obvious cause on initial
evaluation were included
All patients of AECOPD (irrespective of presence or absence
of PE) were classified as having high risk for PE based on
SGS. However, patients with PE had significantly higher
D-dimer, CUS/Doppler (Lower values compared to patients without PE (5.57 ± 1.158 in
limbs and pelvis) and MDCT-PA
patients with PE vs. 3.49 ± 0.592 in patients without PE,
-ve CUS/Doppler P < 0.001).
+ve MDCT-PA and/or
and MDCT-PA CUS/Doppler and
+ve CUS/Doppler plus No significant difference was observed between two
high pretest probability and groups in terms of age, sex distribution, and risk factors
contraindication to MDCT-PA
for embolism except for previous history of VTE (35.7%,
5/14 in patients with PE vs. 12.8%, 11/86 in patients with
No pulmonary Pulmonary Pulmonary no PE, P = 0.03) [Table 1].
embolism embolism embolism
(n = 86) (n = 1) (n = 13)
Significant difference was observed in clinical
presentation and vital signs among patients of AECOPD
Figure 1: Flow chart of the study protocol with and without PE. Hemoptysis was present in
35.7% (5 out of 14) of patients with PE and only
protocol. AECOPD was managed as per the available GOLD in 7% (6 out of 84) of patients with no evidence of
guidelines.[20] PE (P = 0.001). Chest pain was the presenting complaint
in 92.9% (13 out of 14) of patients with PE compared to
Ethics and consent 38.4% (33 out of 84) of patients with no PE (P = 0.001).
The study protocol was approved by departmental ethics Patients with PE were more likely to have tachycardia
(heart rate [HR] >100/min), tachypnea (respiratory
committee. A written consent was obtained from all
rate [RR] >30/min), and hypotension (systolic blood
patients who participated in the study.
pressure [SBP] <100 mmHg) on presentation as
compared to patients with no evidence of PE. No
Statistical analysis
significant difference was observed in terms of laboratory
All continuous variables were expressed as the
parameters between the two groups, except patients with
mean ± standard deviation in case of normally
PE tend to have respiratory alkalosis (pH >7.45: 78.6%
distributed data and were compared using unpaired
vs. 4.3% P ≤ 0.001 and PCO2 ≤45: 71.4% vs. 3.4%
Student’s t‑test. The difference between the two groups
P ≤ 0.001) and low platelet count (<1.5 l/cumm: 85.7%
was assessed using Chi‑square or Fisher’s exact test.
vs. 36.6%, P ≤ 0.001). Qualitative D‑dimer assay was
Multiple logistic regression analysis was performed to
done in all the participants. No difference was observed
identify the predictors of PE. A P < 0.05 was considered
in terms of percentage of positive Dimer test in both
to indicate significance. Statistical analysis was the groups (92.85% in patients with PE vs. 90.6% of
performed using SPSS version 20.0 (SPSS Inc., Chicago, patients without PE, P = 0.694) [Table 1]. The presence
Illinois, USA). of previous history of VTE, hemoptysis, chest pain,
simplified Geneva score of more than 5, disproportionate
RESULTS tachypnea (RR >30/min), tachycardia (HR >100/
min), hypotension (SBP <100 mmHg), and respiratory
The 100 cases included 57% (n = 57) were males alkalosis were significantly associated with PE in
and 43% (n = 43) were females with a mean age of patients with AECOPD on univariate analysis [Table 3].
66.32 ± 14.06 years. Majority of the patients (69%) However, on multivariate binary logistic regression, the
belonged to age group of more than 60 years with no presence of respiratory alkalosis with PCO2 <45 mmHg
difference between the two groups. The demographic data and pH >7.45 predicted PE in patients with AECOPD.
of the participants are depicted in Table 1.
Management of pulmonary embolism and outcome
PE was observed in 14% (n = 14) of participants. CTPA Out of 13 cases of AECOPD with PE, 38.46% (n = 5)
for PE was positive in 13% (n = 13) of cases, while as one fulfilled the criteria for thrombolysis. Majority of these
patient died before CTPA was done but had DVT on CUS/ patients (80%, n = 4) had thrombus in main pulmonary
Doppler. Among the participants with PE, 63% (n = 9) artery. Streptokinase infusion was used as an agent
had the concomitant presence of lower extremity DVT. In for systemic thrombolysis in 4 (80%) patients and
majority of the patients (46%) with PE, thrombus was seen t‑PA in 1 (20%) patient. Four out of five (80%) patients

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 Chaudhary, et al.: Prevalence and predictors of PE in patients with AECOPD

Table 1: Comparison of patient characteristics between acute exacerbation of chronic obstructive pulmonary disease
with and without pulmonary embolism
Patient characteristic AECOPD with PE (n=14), n (%) AECOPD with no PE (n=86), n (%) P
Age in years
<60 3 (21.4) 28 (32.6)
≥60 11 (78.6) 58 (67.4) 0.404
Gender
Male 7 (50) 50 (58) 0.750
Female 7 (50) 36 (42) 0.750
Smoking 12 (85.7) 65 (75.58) 0.403
Risk factors for PE
Recent surgery 4 (28.5) 20 (23.2) 0.750
Recent trauma 3 (21.4) 16 (18.6) 0.900
Active malignancy 3 (21.4) 11 (12.8) 0.500
Previous history of VTE 5 (35.7) 11 (12.8) 0.030
Comorbid illnesses
Hypertension 13 (92.85) 48 (55.8) 0.008
Diabetes mellitus 3 (21.42) 26 (30.2) 0.5008
Obesity 3 (21.42) 24 (28.9) 0.612
Stage of COPD (GOLD)
Stage II 3 (21.43) 30 (34.9) 0.320
Stage III 10 (71.43) 47 (54.6) 0.239
Stage IV 1 (7.14) 8 (9.30) 0.793
Clinical symptoms and signs
Hemoptysis 5 (35.7) 6 (6.9) 0.002
Chest pain 13 (92.8) 33 (38.3) 0.001
Respiratory rate >30/min 14 (100) 36 (43.4) 0.001
Hypotension (SBP <100 mmHg) 9 (64.3) 1 (1.2) 0.001
Pulse >100 bpm 13 (92.9) 24 (28.9) 0.001
Simplified Geneva Score 5.57±1.158 3.49±0.592 <0.001
Laboratory and blood gas values
Polycythemia 8 (57.14) 27 (31.4) 0.06
Total leucocyte count
<4000/µL 0 (0) 0 (0)
4000-10,000/µL 0 (0) 0 (0)
>10,000/µL 14 (100) 84 (100) ns
Platelet count
<150 ×103/µL 12 (85.71) 33 (38.37) 0.0096
>150 ×103/µL 2 (14.28) 53 (61.62)
Positive D dimer 13 (92.8) 78 (90.6) 0.694
Arterial blood gas values
Oxygen saturation (mean±SD) 73.6±8.38 73.84±8.12 0.814
paO2, mmHg (mean±SD) 50±8.6 49.9±8.48 0.548
paCO2, mmHg (mean±SD) 47.3±5.66 61.4±7.38 <0.001
pH (mean±SD) 7.46±0.064 7.36±0.063 <0.001
pH >7.45 11 (78.6) 4 (4.7) <0.001
PCO2 (<45 mmHg) 10 (71.42) 3 (3.48) 0.001
In hospital mortality 2 (14.28) 5 (5.81) 0.249
PE: Pulmonary embolism, COPD: Chronic obstructive pulmonary disease, AECOPD: Acute exacerbation of COPD, SD: Standard deviation, SBP: Systolic
blood pressure, VTE: Venous thromboembolism

who received thrombolysis improved clinically with The prevalence of PE in COPD patients with unknown
hemodynamic stability. Remaining patients of PE (n = 8) etiology varies from as low as 2% to as high as 29.1%.[11,21‑27]
who did not require thrombolysis were managed with Tillie‑Leblond et al. reported that 15 out of 60 (25%)
anticoagulation alone in addition to standard of care for patients with AECOPD of unknown etiology had PE.
the management of AECOPD. Total of eight patients died Similarly, Gunen et al. reported 29.1% prevalence of PE in
during hospitalization. No significant difference was noted patients with AECOPD of unknown reason. However, in a
with regard to the in‑hospital mortality between the two study by Rutschmann et al., the prevalence of PE was only
groups (5.81%, n = 5 in patients without PE vs. 14.28%, 3.3%. The low prevalence of PE might be due to selection
n = 2 in patients with PE, P = 0.25). bias excluding patients with D‑dimer level <500 µg/l and
with low clinical probability of PE. A study from India
DISCUSSION and Korea reported the prevalence of PE to be 2% and
5%, respectively. In a meta‑analysis that included seven
The present study showed the prevalence of PE in studies have shown that the pooled prevalence of PE
patients with AECOPD of unknown etiology to be 14%. in unexplained AE‑COPD was 16.1% (95% confidence

536 Lung India • Volume 38 • Issue 6 • November-December 2021

 Chaudhary, et al.: Prevalence and predictors of PE in patients with AECOPD

Table 2: Findings of computed tomographic pulmonary was more likely to be associated with PE (P value 0.04,
angiogram in patients with acute exacerbation of chronic RR 0.26, 95% CI, 0.07–0.93).[23,32] Tillie‑Leblond et al.
obstructive pulmonary disease of unknown etiology reported that in addition to previous history of VTE,
Findings on CTPA n (%) presence of malignancy was associated with higher risk
No evidence of pulmonary embolism 86 (86) of PE (risk ratio, 1.82 [CI, 1.13–2.92]).[21] Laurent B et al.
Evidence of thrombus in pulmonary arteries 13 (13) concluded that COPD patients with a history of venous
Central thrombus 6 (46.1)
Segmental thrombus 5 (38.5)
thromboembolism, especially previous PE has increased
Subsegmental thrombus 2 (15.4) risk of recurrence of PE and fatal PE as compared to those
CTPA: Computed tomographic pulmonary angiogram
presenting with DVT alone.[14]

The most common symptom of PE is breathlessness at

Table 3: Factors associated with high risk for pulmonary
rest and with exertion, orthopnea, pleuritic chest pain,
embolism in patients with acute exacerbation of chronic
obstructive pulmonary disease by univariate analysis wheezing, cough, and hemoptysis, whereas the most
Patient characteristic (n) OR 95% CI (lower P
common signs include tachypnea, tachycardia, decreased
limit-upper limit) breath sounds, or accentuated second heart sound.[33,34]
Previous history of VTE 3.79 1.07-13.39 0.050
Hemoptysis 7.40 1.88-29.22 0.005 Although symptoms of AECOPD due to PE are nonspecific,
Chest pain 20.88 2.61-167.10 0.001 previous studies have reported that chest pain was more
Tachypnea (respiratory rate >30/min) 31.72 3.93-255.57 0.001 frequently reported by patients of AECOPD with PE as
Hypotension (SBP <100 mmHg) 40.24 4.96-326.18 0.001 compared to patients with no PE.[22,23,31] Our study revealed
Tachycardia (pulse >100 bpm) 31.72 3.93-255.57 0.001
PCO2 (<45 mmHg) 69.17 13.49-354.58 0.001
that, among clinical features, the presence of pleuritic
pH >7.45 75.16 14.81-381.293 0.001 chest pain and hemoptysis significantly predicted PE as
Platelet (<150,000 mm3) 10.65 2.23-50.67 0.001 a cause of AECOPD compared to other symptoms (P=).
SBP: Systolic blood pressure, VTE: Venous thromboembolism, OR: Odds However, few studies have failed to show any significant
ratio, CI: Confidence interval difference of symptoms in patients of AECOPD with and
without PE.[21,34] The result of a recent meta‑analysis that
interval [CI]: 8.3%–25.8%).[10] These differences could be evaluated the prevalence of PE in patients of unknown
due to number of reasons that may include difference in etiology showed that, in patients with AE‑COPD, the
sample size, enrollment criteria, study design, or diagnostic presence of pleuritic chest pain significantly predicted
modalities used (V/Q scan vs. CTPA). the presence of PE.[10]

Various validated bedside clinical prediction scores are Patients with peripheral pulmonary embolus usually
present with chest pain and hemoptysis. In a series of
being used to predict the likelihood of PE and to reduce the
172 patients who presented with AECOPD secondary to
need for imaging.[28,29] We observed that the use of clinical
PE, the most common symptom reported was pleuritic
prediction score (simplified Geneva score) was not useful
chest pain. About 80% of patients with PE had peripheral
in predicting PE in patients with AECOPD. In our study,
pulmonary embolus.[31] However, contrary to this, our
all patients with AECOPD had simplified Geneva score
study reported that 92.8% (n = 13) of patients with
of >2, indicating high likelihood of PE, but only 13% of
CTPA documented PE, presented with chest pain and
patients (13/100) had evidence of PE. However, a significant
42.8%of these had centrally located thrombus. Similar
difference was noted in patients with and without PE if findings were reported by Gunen et al. in his study.[22]
mean values of SGS were considered (5.57 ± 1.16 in These findings can be explained by the fact that massive
patients with PE vs. 3.49 ± 0.59 in patients without PE, centrally located PE can cause ischemic chest pain from
P ≤ 0.001). Therefore, likelihood of PE was significantly right ventricular infarction.
higher in patients of AECOPD with SGS of more than 5.
Gunen et al. reported that none of the patients with low There was a significant difference in terms of physical
clinical prediction score and about 20% of patients with examination findings in patients of AECOPD with
moderate score had PE. However, various studies have a n d w i t h o u t P E . Ta c h y c a r d i a ( H R > 1 0 0 / m i n ) ,
shown that patients of COPD with PE had lower pretest tachypnea (RR > 30/min), and hypotension (SBP
probability for PE using various PE predicting scores.[22,30,31] of < 100 mmHg) was present in significantly higher
These observations showed that the use of clinical percentage of AECOPD patients with PE compared to
prediction scoring system can be misleading when used patients with no PE. Our findings were in consistent
in patients of COPD in predicting PE. with those reported by previous studies. [26,35] Hence,
the suspicion of PE should be kept higher in patients of
We did not observe a significant association of PE AECOPD with disproportionate tachycardia, tachypnea,
in patients with AECOPD of unknown etiology with and hypotension.
well‑known risk factors except previous history of VTE.
Studies have shown that, among various risk factors for Patients of COPD with acute exacerbation may present
PE, the presence of previous history of venous thrombosis with either hypercapnic or hypoxemic respiratory failure.

Lung India • Volume 38 • Issue 6 • November-December 2021 537

 Chaudhary, et al.: Prevalence and predictors of PE in patients with AECOPD

In the acute setting, hypercapnea may be increased true burden of the disease so as to modulate the management
secondary to increased dead space ventilation and accordingly.
ventilation/perfusion (V/Q) mismatch caused by increased
mucus production and bronchial constriction. In patients CONCLUSION
with PE, ABG usually reveals hypoxemia, hypocapnia,
and respiratory alkalosis.[36,37] We observed that patients PE was responsible for AECOPD in a significant number of
of AECOPD with PE had significantly lower levels of patients (14%) with no obvious cause on initial assessment.
paCO2 and higher pH compared to patients with no PE. The presence of PE should be considered in patients of
These findings may be due to reflex tachypnea associated COPD who present with acute worsening of their symptoms
with PE secondary to increase in dead space ventilation. particularly when there is the presence of risk factors for
Our findings were in consistent with those reported by DVT and clinical manifestations consistent with acute PE.
Tillie‑Leblond et al., they observed that a decrease of
paCO2 of at least 5 mmHg from baseline was the only Financial support and sponsorship
ABG abnormality associated with PE.[21] Rodger et al. Nil.
and Lippmann and Fein. also suggested that a decrease
in paCO 2 during COPD exacerbation might indicate Conflicts of interest
PE.[33,38] On the other hand, no reduction in paCO2was There are no conflicts of interest.
reported in patients of AECOPD with PE by Lesser et al.
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