1. A Case of Pulmonary Embolism; Medical Student’s Experience
By: Muhamad Na’im B. Ab Razak
Medical student of University Science of Malaysia
Case Summary
53 Years Old Malay Lady who was recently findings and A-a gradient. Therefore, CT
discharge from ward with problem list of Angiography was done and showed feature
morbid obesity, uncontrolled diabetes of extensive pulmonary embolism.
mellitus, hyperlipidaemia and hypertension
presented to emergency department with the IV streptokinase 250 000 unit stat was
chief complaint of sudden onset severe commenced and followed with
shortness of breath associated with central Streptokinase IV infusion 500 000 unit in 50
pleuritic chest pain and diffuse sweating. ml normal saline and patient was transferred
to Cardiology Care Unit for further
She was alert and oriented to the time, place management.
and person. Her blood pressure was 180/88
mmHg, heart rate was 120 b.p.m and
respiratory rate was 20 breath per minute.
Full blood count, Renal Function Test were
inconclusive. Cardiac biomarkers were not
elevated, D Dimer was >5000 ng/ml.
ECG shows classical feature of Pulmonary
embolism which are tachycardia, Deep S
wave in lead I, Deep Q wave in lead III and
inverted T wave in lead III (S1Q3T3)
ABG under high flow mask of 100%
oxygen, 10 L/min showed pH of 7.4, PCO2
28.6 mmHg, PO2 131 mmHg,HCO3- 19.6
mmol/L. Calculated Alveolar-arterial
gradient (A-a gradient) was 190 which Fig 1: Urgent CTA of thorax shows good
suggestive of V/Q mismatch. opacification of pulmonary trunk but
inhomogenous opacification of bilateral right
and left main pulmonary artery with filling
A diagnosis of Pulmonary embolism was
defect seeing within. Radiological diagnosis of
made based on high index of suspiciousness
pulmonary embolism was made by radiologist.
in risk factor, clinical presentation, ECG

2. Fig 2: ECG shows Tachycardia, Deep S wave in lead I, Deep Q wave in lead III and inverted T
in
wave in lead III (S1Q3T3)
Discussion.
Pulmonary embolism (PE) is not a disease this non perfused lung will no longer
per se but often a complication of other secretes surfactant and cause alveolar
al
vascular problem particularly deep vein collapse which exacerbates the hypoxemia.
thrombosis. The devastating consequence of
ing The non perfused lung tissue however
this disease is mainly resulting from the seldom become infarcted because of
difficulty in establishing the diagnosis due to continuous oxygen supply by bronchial
nonspecific signs and symptoms. . circulation and airways.
Mortality in untreated PE is approximately The European Society of Cardiology has
30%, but with adequate (anticoagulant) classified PE into two main groups which
treatment, this can be reduced to 2
2–8%. [A. are massive and non-massive. Massive PE
massive. M
Torbicki et al] consists of shock and/or hypotension
(defined as a systolic blood pressure <90
PE occurs when when one or more mmHg or a pressure drop of 40 mmHg for
pulmonary artery being blocked by blood >15 min if not caused by new-onset
new
clots that dislodged from peripheral vein If
vein. arrhythmia, hypovolumia or sepsis).
volumia
the blockage occurs at the bifurcation of the Otherwise non-massive PE can be
massive
main pulmonary artery, then it is called diagnosed.
saddle pulmonary embolism
In other words, massive PE also defined as
The blockake cause V/Q mismatch in which embolus causing sufficient obstruction to
the lung tissue is ventilated but not perfused. pulmonary flow to result in hemodynamic
This will give rise to intrapulmonary dead instability, right ventricular failure, and
space and impair gas exchange. After hours, hypoxemia [Paul Maggio et al]

3. Virchow’s triad consist of stasis of the
blood, hypercoagulable state and endothelial Wells score for Probability of PE
damage has been attributed to the deep vein Criteria Points
thrombosis and PE. This condition can be Clinical signs of DVT +3
due to blood and blood vessel disorder, Alternative diagnosis less +3
probable than PE
prolong immobilization, prolong surgery,
Heart rate > 100 b.p.m +1.5
pregnancy, oral contraceptive and estrogen Immobilization or surgery < +1.5
replacement, and malignancy. 4 Weeks ago
Previous DVT or PE +1.5
Even though the signs and symptoms for PE Haemoptysis +1
are not specific, Prospective Investigation of Cancer +1
Pulmonary Embolism Diagnosis (PIOPED)
Table 1: Total score: <2 indicates a low probability of PE;
study found out that the most common 2–6 indicates a moderate probability of PE; >6 indicates a
presentation are dyspnea (73%), pleuritic high probability of PE
chest pain (66%), cough (37%), and
hemoptysis (13%) [Nader Kamangar].
ECG is a poor diagnostic tool for PE and it
Other atypical symptoms include seizure,
is rather being used to rule out other
syncope, abdominal pain, fever, productive
potential life threatening diagnosis such as
cough, wheezing, altered sensorium, new
myocardial infarction. [Chan TC et al]. The
onset atrial fibrillation, and flank pain.
ECG is often abnormal in PE however, the
findings are not sensitive and not specific.
In a time without or not readily accessible
[Chan TC et al]. T-wave inversion in the
CT angiography, few scoring system has
precordial leads is the most common
been develop to predict the possibility of PE
abnormality (68%), and represents the ECG
with the famous scoring system being
sign best correlated to the severity of the
Geneva score and Wells score. However,
PE.[Emile Ferrari et al]. In the same study,
both of this scoring system has not been
Emile Ferrari et al found out that Anterior T
validated and derived from selected
wave inversions had a sensitivity of 85%
population.
and specificity of 81% for massive PE. The
so called classical ECG manifestation of PE
Therefore, diagnosis of PE should be made
which is the SI Q3 T3 pattern was described
based on high level of suspiciousness in the
by McGinn and White in the year of 1935.
presence of risk factor and clinical
However, it is not a pattern that characterize
manifestation.
the pulmonary embolism alone but rather
sign of acute cor pulmonale. Therefore,
Chest X Ray is not really help in detecting
other causes giving rise to cor pulmonale
PE but it may show Westermark sign,
such as acute bronchospasm and
Hamptom Hump and pulmonary effusion.
pneumothorax may as well give this ECG
However, it is good to rule out other causes
pattern. Apart from that, ECG findings often
of dyspnoe.
shows tachycardia.

4. D Dimer is a degradation product of pulmonary arterial pressure. A typical
crosslinked fibrin. Previously, it is being echocardiographic picture of
used as one of the main screening haemodynamically significant PE includes
investigation for PE. However, it has less dilated, hypokinetic RV, an increased
positive prediction value in diagnosing PE. RV/LV ratio caused by interventricular
A level of D- Dimer below than 500 µg . l-1 septal bulging into the LV, dilated proximal
is a cut off point to safely excludes PE. pulmonary arteries, increased velocity of the
jet of tricuspid regurgitation (usually in the
There is a practice among the clinician to range of 3–3·5 m s-1), and disturbed flow
calculate alveolar-arterial gradient in order velocity pattern in the RV outflow tract.
to establish the diagnosis of PE. This value, Furthermore, the inferior vena cava is
can be calculated based on ABG result using usually dilated and does not collapse on
the below formula. Normal adult A-a inspiration. [A. Torbicki et al]
gradient is 20. However, Marc A. Rodger et
al found out that none of the ABG data or The gold standard for diagnosing pulmonary
prediction rules had sufficient negative embolism is CT Angiography. CT has
predictive value, specificity, or likelihood become the first-line modality for imaging
ratios to be useful in the management of in patients suspected of having PE. CT is
patients with suspected PE. Therefore, they now an attractive means for establishing a
conclude that ABG data alone or in safe, highly accurate, and cost-effective
combination with other clinical data are not diagnosis of PE. [U.J Schoepf & P.
useful in the assessment of suspected PE. Costello]. However, according to cohort
study by M. J. L. Van Strijen et al, the
sensitivity of spiral CT was 86% for
A-a gradient = PAO2 − PaO2 segmental or larger PE and 21% in the group
of patients with subsegmental PE.
[FiO2*(Patm-PH2O)-(PaCO2/0.8) ] - PaO2 Therefore, they draw a conclusion that in
patients with clinically suspected PE and an
PAO2 = alveolar PO2 (calculated from the
abnormal perfusion scintigraphy, single-
alveolar gas equation)
slice detector spiral CT is not sensitive
PaO2 = arterial PO2 (measured in arterial enough to be used as the sole test to exclude
blood A-a gradient) PE.
= ( 760 - 47 ) x FiO2 - PaCO2 /0.8 (or 1)
Doppler ultrasound is both 95% sensitive
and specific in detecting deep venous
thrombosis above the knee if DVT is
Table 2 A-a gradient
suspected as causes of PE.
Echocardiography may suggest or reinforce
clinical suspicion of PE if right ventricular
(RV) overload and dysfunction is found in
the presence of Doppler signs of increased

5. In the recent guidelines of the American Besides thrombolytic therapy, other
College of Chest Physicians, either LMWH management includes, high flow oxygen
or UFH is recommended for the initial supply, continuous vital sign monitoring
treatment of venous thromboembolism. In particularly SPO2, heart rate and BP,
patients with advanced renal insufficiency, measures to prevent or control the effect of
the recommendation is to use UFH rather acute circulatory failure like infusion of
the LMWH. [GF Pineo& RD Hull]. Dobutamine and dopamine. The usefulness
of fluid challenge is controversial and
Vitamin K antagonists (VKAs) are the should not exceed 500 ml. as it may
agents of choice for long-term treatment and deteriorate the condition of the patient.
secondary prophylaxis of pulmonary
embolism (PE), as they were shown to be Acute pulmonary thrombectomy has a
effective in preventing recurrence of the limited role in massive, life-threatening PE.
disease [G Agnelli & C Becattini]
Reference
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