Pulmonary embolism (PE) is the sudden, total or partial obliteration of the trunk of the pulmonary artery or one of its branches by a blood clot, most often resulting from deep vein thrombosis (DVT) [1][2]. PE is common in developed countries and is the 3rd most common acute cardiovascular syndrome after myocardial infarction and stroke [3]-[5]. In France in 2010, the incidence of PE was 85.8 cases per 100,000 inhabitants [6]. In Africa, data on venous thromboembolic (VTE) diseases are still difficult to obtain and the frequency is often underestimated because of difficulties linked to the scarcity of diagnostic resources [7][8]. In 2019, in a study carried out in the southern part of Togo, Pessinaba et al. reported a frequency of 5% for severe PE [9]. PE is said to be severe when it is associated with shock or haemodynamic instability [10][11]. The 3-month mortality rate for severe PE is very high, approaching 50%, with most deaths occurring immediately after diagnosis, justifying emergency treatment with drugs, intervention or surgery [12][13]. Data on severe PE are even rarer, especially in developing countries. This explains the rationale behind this study of severe PE in a specialised department, the objectives of which were to determine its prevalence in hospitals and to describe its epidemiological, diagnostic, therapeutic and evolutionary characteristics.

We carried out a descriptive cross-sectional study on one of the most life-threatening cardiovascular emergencies, severe PE, the management of which consists of unblocking the occluded pulmonary artery. The aim of this study was to investigate the epidemiological, diagnostic, therapeutic and evolutionary aspects of severe PE in a specialised department. The prevalence of severe PE as a proportion of all PE was 30.9%, with a strong female predominance. This high proportion of severe pulmonary embolism is found in almost all studies conducted in the sub-region, such as Houenassi et al. in Benin (38.46%) and Pessinaba et al. in Togo (27.5%) [9][14]. This high rate of severe PE is thought to be due to delayed diagnosis. In Western countries, however, the proportion of severe PE is much lower, at around 5% [15]. Patients with severe PE on the African continent are relatively younger than those in Western countries, where life expectancy is higher [6]-[16]. In our study, we noted a strong female predominance, in line with the findings of most authors [9][17][18]; however, some authors have also reported a male predominance in their series [14]. In our study, we noted a large number of PE cases between November and May. This period of the year is characterised by high temperatures in our country, which suggests that heat could be a factor favouring thrombus formation.

PE is often promoted by factors that may be transient or permanent. In our study, neoplastic factors were the most common, accounting for 23.1% of cases. This rate is similar to general data on the causes of venous thromboembolic disease (VTE), which estimates that 20% of patients with VTE have an active cancer [19]. Higher rates of active cancer (40%) have been reported by some authors, particularly for specific sites such as thrombosis of the upper limb [20]. Classically, cancer is involved in the development of VTE through the three mechanisms of Virchow’s triad: blood stasis through immobilisation or compression, hypercoagulability through activation of coagulation factors, and damage to the vascular endothelium through the effects of chemotherapy and other therapeutic techniques [19].

Generally, the clinical diagnosis of severe PE is classic, with symptoms such as dyspnoea and chest pain in the presence of VTE risk factors associated with signs of cardiogenic shock. In our study, these two symptoms were reported in 92.3% and 53.8% of cases, respectively. Pessinaba et al. in Togo and Adam et al. in Chad also found dyspnoea and chest pain to be the most frequent symptoms [17]-[21]. Syncope is one of the signs of severity, but it is not sufficient in itself to indicate a PE with a high mortality risk [22]. Syncope was 38.5% in our study but may also be rarer as in the series by Doghmi et al., who reported no cases of syncope in a sample of 20 patients with severe PE [23].

From a paraclinical point of view, the signs indicative of PE was found in almost all the patients, reflecting a delay in diagnosis related to the delay in consulting the patients. The most frequent electrocardiographic signs were sinus tachycardia, anteroseptal subepicardial ischaemia, intraventricular conduction abnormalities and right axial position, found in 92.3% of patients. As for the echocardiographic signs of acute pulmonary heart disease (dilatation of the right cavities with ventricular systolic dysfunction, pulmonary arterial hypertension, paradoxical septum and McConnell 60/60 sign), they were found in 100% of cases. All these signs have been described in the literature as signs of severe PE when associated with shock or haemodynamic instability [10][24]. Venous Doppler of the lower limbs showed a high rate of thrombosis (100%) compared with Doghmi et al. in Morocco, who found only 50% thrombosis in patients with severe PE [23]. Thoracic angioscan is the test of choice for confirming PE, but in the event of haemodynamic instability or shock, the discovery of a thrombus in the peripheral veins or right heart chambers can confirm the diagnosis of PE [2][10]. In our study, the presence of thrombus in the right heart chambers in three patients led to the conclusion of PE, while angioscan was only performed in 10 patients. The thrombus was proximal in all ten patients and bilateral in half (5 patients). These results corroborate data in the literature according to which the more proximal and bilateral the thrombus, the worse the prognosis, since the mortality rate is very high, approaching 50% during the first three months [12][13].

Treatment of severe PE is an emergency and consists of unblocking the occluded artery by medication (thrombolysis), intervention (thrombectomy, thromboaspiration) or surgery (embolectomy). However, in developing countries such as Togo, the treatment most often available is thrombolysis with first-generation molecules such as streptokinase. This is the molecule received by all our patients (12 patients) according to the short protocol at a dosage of 1.5 million, offering efficacy and safety comparable to those of alteplase [25]. Apart from thrombolysis, the treatment of severe PE consisted of ensuring good oxygenation and maintaining good haemodynamic stability by administering vasopressor amines as required. The in-hospital outcome in our study was marked by a high mortality rate of over 30%. The mortality rate in our study is higher than that of Pessinaba et al. in Togo, who reported a mortality rate of 13.6% [9]. The high mortality rate in our department is explained by the delay in treatment (diagnostic delay due to the very long admission time and therapeutic delay due to patients’ difficulties in honouring thrombolytics). In developed countries, however, where treatment conditions are better, mortality rates are even lower [2][10].

Limitations: Small sample size and retrospective nature of our study.

Severe pulmonary embolism is a frequent medical emergency in our department. The majority of patients were over 50 years of age and predominantly female. There was a long delay in admitting patients to the department with the classic clinical signs of pulmonary embolism. Ultrasonographic signs of acute pulmonary embolism were present in all patients. Streptokinase was the only thrombolytic used. In-hospital mortality was high, reflecting the delay in management. Better organisation of care services and improved technical facilities are needed to improve patient prognosis.