The dilemma in the management of haemodynamically stable pulmonary embolism with right heart thrombus

Abstract

Right ventricular thrombus (RVT) can be life-threatening, since it has the potential to embolise and cause saddle pulmonary embolism (PE). We present a patient who initially presented with haemodynamically stable PE with evidence of RVT on echocardiogram. She was placed on heparin drip; however, she later developed cardiac arrest and died due to embolisation of RVT to the pulmonary vasculature. Although management of haemodynamically stable PE in patients with RVT is still a matter of debate, ¹ given the outcome we suggest that thrombolysis or emergent embolectomy at the presentation, in this case, may have had a favourable outcome.

Background

Right ventricular thrombus (RVT) is an uncommon complication which occurs in approximately 4% of patients with pulmonary embolism (PE). The mortality risk is higher in acute PE with RVT compared with PE with no RVT.² Guidelines for management for haemodynamically stable PE with RVT has not been well defined and is still a matter of debate.¹ The outcome of our case suggests performing thrombolysis for patients presenting with haemodynamically stable PE and RVT may have a more favourable outcome.

Case presentation

A woman in her 80’s presented to the emergency department with complaints of acute shortness of breath and sudden onset pleuritic chest pain. Her vitals were remarkable for tachycardia and tachypnea; however, her blood pressure was within normal limits. She scored 6 (heart rate >100, based on symptoms PE is #1 diagnosis or equally likely, due to a history of Alzheimer’s she has been less mobile) on Well’s criteria which suggested PE be likely. Thus, provoked PE was suspected; however, due to the presence of an acute kidney injury, a ventilation–perfusion scan was performed instead of a CT angiogram (CTA). It showed a high probability of PE with multiple mismatched perfusion/ventilation defects (figure 1). We performed an echocardiogram which showed a sessile, well-organised mobile echodensity in the right ventricle attached to the ventricular wall or chordae and extending into the right ventricular outlet measuring approximately 1×2 cm. However, there was no evidence of right heart strain (figure 2). We then started her on a heparin drip based on recent recommendations.^1–3 The next afternoon, there was a sudden drop in O₂ saturation to ~70%, which was improved to ~80% with supplemental oxygenation, and she also had tachycardia at 100 bpm. However, her blood pressure was within normal limits. We obtained an emergent repeat echocardiogram, which did not show the previously seen RVT, suggesting its migration to the pulmonary vasculature (figure 3).

Figure 1.

Ventilation–perfusion scan showing a high probability of pulmonary embolism with multiple mismatched perfusion–ventilation defects.

Figure 2.

An echocardiogram showing a sessile, well-organised mobile echodensity in the right ventricle attached to the ventricular wall or chordae and extending into the right ventricular outlet measuring approximately 1×2 cm.

Figure 3.

Emergent repeat echocardiogram showing the disappearance/migration of previously seen right ventricular thrombus into the pulmonary vasculature.

Furthermore, there was also evidence of right heart strain with severely elevated right ventricular systolic pressure suggesting significant clot migration, causing a saddle emboli. An emergent CTA of the chest was immediately ordered to determine the location of the PE to perform catheter-directed thrombolysis. However, soon afterwards, she lost her pulse, and we immediately initiated cardiopulmonary resuscitation (CPR). During resuscitation, she received systemic thrombolysis with alteplase.

Outcome and follow-up

Despite resuscitation efforts with CPR and thrombolysis, a return of spontaneous circulation could not be achieved and she was pronounced dead after 35 min.

Discussion

Right heart thrombi (RiHT) is associated with 2.5%–4.5% of patients with PE.1 2 4–6 Younger age, previous history of bleed, congestive heart failure, cancer, syncope, systolic blood pressure <100 mm Hg and arterial oxyhaemoglobin saturation <90% had increased incidence of PE with RiHT.⁴ Furthermore, hypotension is known to complicate PE in about 14% of cases with RVT as opposed to 4% of cases of PE without RVT.⁴

In a study from the International Cooperative Pulmonary Embolism (ICPE) registry which described 42 cases of RiHT, the mortality rate was 21% and 29% at 14 days and 3 months, respectively, compared with the mortality rate of 11% and 16%, respectively, in cases with PE without RiHT.⁴ The above was supported by the RiHTER study and a meta-analysis by Barrios which demonstrated that patients with a RiHT and PE had a significantly higher mortality rate as compared with PE with no RiHT (19% vs 8%, respectively, p=0.003 in the RiHTER study and 3.0 fold in the meta-analysis by Barrios).^{2 4}

Optimal therapy for PE with right ventricular thrombi has not been well defined and treatment selection is still a subject of debate. A study by Barrios et al which included 325 patients with RiHT showed that reperfusion therapy compared with anticoagulation was associated with improved survival; however, the results were not statistically significant.⁷ Therefore, the study recommended against using interventions such as thrombolysis and embolectomy in haemodynamically stable patients with PE and RiHT.^{3 7} Contrarily, Koć suggested that surgical removal of thrombus should be strongly considered when RiHT is protruding via PFO into the left atrium¹ since PFO was reported to be a risk factor for acute ischaemic stroke in PE patients presenting with right ventricular overload.^{8 9}

The results from the ICPE registry study showed a mortality of 20.8%, 23.5% and 25% for cases of RiHT treated with thrombolysis, heparin alone and surgical embolectomy, respectively.^{1 4} Another retrospective study, which analysed 177 cases of RiHT, showed a mortality of 100%, 28.6%, 23.8% and 11.3% in cases with no therapy, anticoagulation, surgical embolectomy and thrombolysis, respectively.^{1 10}

We should also be aware that thrombolysis has a higher bleeding risk compared with heparin alone (21.9% and 7.9% of cases, respectively).¹¹ One of the review articles reported major bleeding as a complication of thrombolysis in 5%–10% cases with the intracranial site being the most common with mortality as high as 50%.¹² Additional studies are warranted to weigh the bleeding risk and survival benefit ratio of thrombolysis compared with heparin alone.

Current literature recommends anticoagulation and intensive care unit transfer for close monitoring of the haemodynamically stable patients with RiHT. Haemodynamically unstable patients and the ones with evidence of right heart strain on the echocardiography should be thrombolysed. Patients with PFO complicating with PE and RiHT should undergo emergent thrombectomy even when haemodynamically stable.¹

Learning points.

• The association of pulmonary embolism (PE) with right ventricular thrombi/right heart thrombi is rare but life-threatening. Data on the optimal management of haemodynamically stable PE with right ventricular thrombus (RVT) are lacking.

• Thrombolysis is recommended for management of haemodynamically unstable PE with evidence of right heart strain on an echocardiogram.

• Further studies with larger patient populations are required to establish treatment guidelines for haemodynamically stable PE with RVT.

• A careful assessment of bleeding risk and survival benefit in such patients should be perfromed while deciding among treatment options.