PULMONARY EMBOLISM

Pulmonary embolism presents with a wide clinical
spectrum, from asymptomatic disease to life
threatening massive PE that causes hypotension and
cardiogenic shock. Several studies have been published,
since the seminal trial that tested anticoagulation
against no therapy12. There is hardly any published data
on PE from India.
The clinical presentation and the investigations
including electrocardiography, chest radiography, and
analysis of arterial blood gases cannot be relied on to
confirm or rule out PE because of lack of adequate
specificity13. The presence of one or more risk factors
may lower the threshold for diagnostic evaluation. This
did not help in the present series as none of the patients
had any obvious risk factor. D-dimer testing has been
reported to have a sensitivity ranging from almost 80-
100 percent. However, in the present series due to the
unavailability of the test at all times, it could be
performed only in six patients and was found to be
positive.
Since the origin of the thrombus is mostly from deep
veins of the legs, compression ultrasound of lower limb
veins is a useful investigation in the diagnosis of PE. It
is, however, reported to be positive only in 10-20% of
patients without leg symptoms or signs who undergo
evaluation and in approximately 50% of patients with
proven PE13. Thus, PE cannot be ruled out on the basis
of negative results on ultrasound. Compression
ultrasound has its value in situations where there is a
high clinical probability of PE and the patient has no
past history of VTE13. In our study, eight patients had
symptoms and signs of DVT, whereas 16 had an
ultrasonographic evidence of DVT. Thus, compression
ultrasound is a useful investigation in patients with
symptomatic PE. Perfusion scan has been used for
almost three decades for the diagnosis of PE and is a
valuable tool when the results are definitive. But
approximately 30-70% of scans are non-diagnostic and
the clinician is left in a diagnostic dilemma of
uncertainty14. Further, it is insensitive in patients with
pre-existing lung diseases, especially the chronic
obstructive lung disease15.
The use of spiral CTPA is a major advancement in the
diagnosis of PE. The sensitivity and specificity for
detection of pulmonary embolus by CTPA at the main,
lobar and segmental levels are greater than 90% with
accuracy decreasing when isolated subsegmental
vessels are involved14. Also, spiral CTPA has a greater
interobserver agreement. With the third-generation
scanners which provide 1-mm resolution in a single
breath hold, the spiral CTPA is now the preferred
Figure 3. Spiral computed tomographic pulmonary angiography
showing isolated subsegmental thrombus.
Figure 4. Computed tomography showing peripheral wedgeshaped
infarct on right side.
respectively (Table).
Massive PE was diagnosed in 10 patients and submassive
PE in five patients, respectively; while nine
patients had minor PE. Of the 15 patients, 14 were
thrombolysed. One patient had only sub-massive PE
without hypoxemia and was, therefore, not
thrombolysed. All the patients received low molecular
weight haparin (LMWH) followed by oral
anticoagulants. Of the 24 patients, 20 (83.4%) recovered
and were discharged from the hospital. Four patients
died, three due to refractory shock and respiratory
failure and one after a massive upper gastrointestinal
114
imaging modality16. In our study, perfusion scans were
performed in 14 patients and CTPA contributed to
diagnosis in 21 patients. Perfusion scans were of high
probability in 11 patients and non-contributory in the
remaining three patients; CTPA confirmed the diagnosis
in these three patients.
Echocardiography is not used routinely in the
diagnosis of PE, but it is a useful tool in identifying high
risk patients such as those with right ventricular
dysfunction, patent foramen ovale, free floating
thrombus and persistent pulmonary hypertension17. All
our patients underwent echocardiography, and right
ventricular dysfunction was identified in 62.5 percent.
Although there is little doubt about the role of
anticoagulation in PE, thrombolysis is a debatable
indication18,19. There is no conclusive evidence till date to
show that thrombolysis reduces mortality in massive
PE, except a small study which consisted only of eight
patients20. Thrombolysis in sub-massive PE is also a
controversial indication. In a large randomised trial in
patients with PE, Konstantinides et al11 randomised 256
patients to receive both thrombolysis and anticoagulation
or anticoagulation alone. There was no
survival benefit but patients receiving anticoagulation
alone required escalation of treatment in form of
secondary thrombolysis, vasopressor requirement and
mechanical ventilation to prevent clinical deterioration.
We had thrombolysed 14 out of the 24 patients (83.4%),
10 with massive PE and four with sub-massive PE. Of
these 14 patients, four died, three from cardiogenic
shock and one from massive upper gastrointestinal
bleed. All the patients received LMWH followed by oral
warfarin. Monitoring of anticoagulation is important
but is not available widely in India. Finger-prick
techniques for monitoring INR are being increasingly
used in the west11 but again are not available in India.
In conclusion, PE is an under recognised and
underdiagnosed clinical problem in India. A high index
of suspicion is necessary to consider the diagnosis, and
the increasing availability of radiographic and nuclear
imaging techniques are likely to improve its diagnosis
in India. Early recognition and aggressive and
appropriate therapy improves outcome in this
potentially fatal condition.
ACKNOWLEDGEMENTS
Authors thank Dr Balamugesh, Dr Shiva, Dr Pralay,
Dr Mahendran, and Dr Shriraam for their constructive
criticism.