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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 6, November/December 2017
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AFRICA
of patients had moderate and intermediate PE probability,
respectively (Table 3).
Laboratory tests deviated from normal in 68% of patients;
their positivity rates and cut-off values are shown in Table 4.
D-dimer, troponin and BNP levels were positive in all tests
with available results. More than half of the patients (54%)
had abnormal results in their arterial blood gasometry (ABG),
namely hypoxaemia in 34% and acute respiratory alkalosis in
20% of patients.
About a quarter of patients (13 patients) had normal chest
radiography. The electrocardiogram was normal in only 22% of
patients and the classic S1Q3T3 pattern was found in only 18%.
RV enlargement (20%) and RV hypokinesia (8%) were the main
echocardiographic findings in our study. We documented the
presence of deep-vein thrombosis by Doppler ultrasound in 20%
of patients.
PCTA changes were correlated with haemodynamic stability
at admission in all patients; 28% had massive PE, of whom 20%
were haemodynamically unstable; 36% had sub-massive PE and
showed a statistically significant rate of haemodynamic stability
at admission (28 vs 8%,
p
=
0.018). In 36% of patients there was
low-risk PE (Table 5). All patients were stratified according to
the pulmonary embolism severity index and 30% of the patients
had a very high risk of mortality (Table 6).
Heparins were the most common form of in-hospital
anticoagulation. Unfractionated heparin was used in 32% of
patients for 5.4
±
2.1 days. Low-molecular-weight heparins
were used in 44% of patients for 6.2
±
3.7 days. Among these
patients, 70% used oral anticoagulation with warfarin and 6%
used new oral anticoagulants (NOAC) (Table 7). Thrombolytic
therapy was used in 18% of the patients. In 12 patients, it was not
possible to determine the type of anticoagulant used or whether
they used thrombolytic therapy, due to the unavailability of data.
There were complications in 38% of the patients; 15 had
respiratory failure requiring mechanical ventilation and seven
had cardiogenic shock (Table 8). The 24-hour and in-hospital
mortality rates were 2.5 and 20%, respectively. There were
15 deaths, of which five occurred in the first 24 hours after
admission.
Considering the study criteria, three patients had a fatal
outcome and were not included (no imaging confirmation of
PE). However, they showed a high clinical probability for PE and
alternative diagnoses were less likely.
Discussion
The study results characterise the clinical profile of patients
with PE admitted at our hospital. The presented data refer to
the current clinical practice without any interference in medical
procedures. The high clinical suspicion associated with the
immediate availability of pulmonary CT angiography and other
diagnostic tests allowed us to confirm PE cases and exclude
other differential diagnoses. This context has added greater
consistency to the study results.
According to Tambe and colleagues in Cameroon,
10
it was
found that PE is not a rare disease in sub-Saharan African
populations. Institutional unavailability of CT angiography may
favour sub-detection of the disease in some geographic areas.
10
The median age observed in our study was 50.5
±
17.8 years,
similar to that described in the EMPEROR study
11
(56.5
±
18.1
years), and lower than some observational studies describing
Table 3. Pulmonary embolism risk stratification according to the
modifiedWells and Geneva revised scoring systems
PE probability
Wells scoring system
n
(%)
Geneva scoring system
n
(%)
Low
7 (14)
5 (10)
Moderate
28 (56)
Intermediate
29 (58)
High
15 (30)
16 (32)
Total
50
50
Table 4. Frequency and positivity of the auxiliary diagnostic
tests in patients with pulmonary embolism
Diagnostic tests
Number (%)
Laboratory tests
White blood cells (
>
10 × 10
9
cells/l)
14 (28)
LDH (
>
400 U/l)
10 (20)
D-dimers (
>
500 μg/l)
4 (8)
Troponins (
>
0.1 ng/ml)
4 (8)
ESR (
>
10 mm in men,
>
20 mm in women)
3 (6)
BNP (
>
500 pg/ml)
1 (2)
Normal
16 (32)
Arterial blood gasometry (ABG)
Hypoxaemia
17 (34)
Acute respiratory alkalosis
10 (20)
Normal
13 (26)
Absent ABG
13 (26)
Chest radiography
Pulmonary parenchymal infiltrates
7 (14)
Hampton sign
6 (12)
Pleural effusion
4 (8)
Cardiomegaly
2 (4)
Pneumothorax
1 (2)
Westmark sign
1 (2)
Changes not related to PE
5 (10)
Normal
13 (26)
Absent chest radiography
12 (24)
Electrocardiogram
S1Q3T3 pattern
9 (18)
Non-specific repolarisation changes
6 (12)
Right bundle branch block
4 (8)
Right ventricular hypertrophy
1 (2)
Right cardiac axis deviation
1 (2)
Sinus tachycardia
1 (2)
Changes not related to PE
6 (12)
Normal
11 (22)
Absent ECG
11 (22)
Echocardiogram
Enlarged right heart chambers with or without thrombus
10 (20)
Right ventricular hypokinesis
4 (8)
Pulmonary hypertension
3 (6)
Persistent foramen ovale
2 (4)
McConnel sign
2 (4)
Changes not related to PE
4 (8)
Normal
9 (18)
Absent echocardiogram
17 (34)
Limb Doppler ultrasound
Deep-vein thrombosis
10 (20)
Normal
33 (66)
Absent Doppler ultrasound
7 (14)
LDH, lactate dehydrogenase enzyme; ESR, erythrocyte sedimentation rate;
BNP, B-type natriuretic peptide.