Management strategies for saddle pulmonary embolism

Saddle pulmonary embolism (SPE) is a rare type of acute pulmonary embolism (PE) that can lead to sudden haemodynamic collapse and death. It is defined radiologically as a thrombus spanning the pulmonary artery trunk and can be mistaken for massive PE, which is defined on the basis of haemodynamic instability. 

Here, we present a case of SPE in a tertiary care setting, providing insights into its clinical presentation and management. The patient, a woman in her 70s, presented with abrupt-onset dyspnoea, chest tightness and dizziness. Elevated D-dimers prompted a CT pulmonary angiography, revealing a saddle thrombus with bilateral emboli. Although initial anticoagulation therapy showed limited improvement, thrombolysis resulted in significant recovery. The patient was subsequently transitioned to a direct oral anticoagulant (DOAC) and discharged with plans for ongoing monitoring. This case highlights the complexities involved in successful management strategies for SPE, offering valuable insights for clinicians.  

Acute pulmonary embolism

Acute pulmonary embolism (PE) poses a potential threat to life and ranks as the third most common cause of cardiovascular death, following ischaemic heart disease and stroke.^1,2,3,4 It represents the most severe manifestation of venous thromboembolism (VTE), carrying substantial risks of morbidity and mortality. When left untreated, the mortality rate for acute PE can reach as high as 30%. However, with timely diagnosis and appropriate treatment, the death rate for diagnosed and treated PE is approximately 8%.⁵

Saddle pulmonary embolism (PE) is a radiological term denoting a large clot that spans the bifurcation of the pulmonary artery trunk, often extending into bilateral main pulmonary arteries.⁶ It occurs in 2.6% to 5.4% of patients with PE.^7,8 The presence of a large central thrombus in saddle PE may cause concern among clinicians, leading them to categorise it as massive PE and admit patients to the intensive care unit (ICU). 

However, it is important to note that ‘massive PE’ is a haemodynamic definition, indicating any PE accompanied by shock and haemodynamic collapse.⁹ Therefore, it is inaccurate to label patients with saddle PE as having massive PE, as there are instances where these patients present with stable haemodynamic values and a relatively benign clinical profile. Saddle PE exhibits diverse characteristics with variable clinical features and outcomes. Limited data are available to guide clinicians in the general management of saddle PE. Some small studies have indicated that saddle PE does not necessarily result in an unfavourable clinical outcome, with mortality rates ranging from 4.5% to 16%.^8,10

Case presentation 

A woman in her 70s presented to the emergency department reporting shortness of breath. In the previous two days she began experiencing a gradual onset of shortness of breath, even at rest, which exacerbated with minimal exertion. She also reported sensations of chest tightness and dizziness. However, she denied experiencing chest pain, orthopnoea, proximal nocturnal dyspnoea, wheezing, ankle swelling, cough or the production of phlegm. Notably, she had recently been discharged from the hospital after being treated for a lower respiratory tract infection, and her recovery was progressing well, with almost complete resolution of infectious symptoms.

Her medical history included well-controlled type 2 diabetes and hypertension. She reported no recent surgeries. Regular medications comprised oral hypoglycaemic (metformin), an angiotensin receptor blocker (losartan) and aspirin (75mg OD). She denied any family history of clotting disorders. Additionally, she was a non-smoker and non-drinker, and she maintained complete independence in terms of mobility.

During examination in the ED she was afebrile, but exhibited a rapid heart rate at 116 beats per minute and a blood pressure of 102/78mmHg. Her respiratory rate was 20 breaths per minute and her oxygen saturation was 92% on room air. Chest auscultation revealed clear air entry in both lungs with no additional sounds. The rest of the examination was unremarkable. 

The results of her routine initial blood investigations are depicted in Table 1. Her initial blood workup revealed elevated D-dimers at > 4.00µg/ml (normal range 0.01 to 1.00µg/ml).

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Given the elevated D-dimers, a CT pulmonary angiography (CTPA) was conducted, revealing a saddle thrombus in the main pulmonary artery along with massive emboli in both the left and right pulmonary arteries, consistent with a diagnosis of pulmonary thromboembolism (see Figure 1). Subsequently, she was started on a daily regimen of subcutaneous tinzaparin at a dosage of 175 IU/kg.

During the initial phase of treatment, there was limited improvement in her symptoms and oxygen requirements. Unfortunately, in the subsequent days she experienced further clinical deterioration despite receiving anticoagulation therapy. Her oxygen needs increased to 55-100% Fi02 as shown in Table 2. Although her blood pressure remained stable, it was towards the lower side at 112/53mmHg. To assess the possibility of further clot propagation, additional imaging with a repeat CTPA was performed as the patient was transferred to a high dependency unit.

The follow-up CTPA (see Figure 2) revealed the persistent presence of a saddle embolus in the main pulmonary artery, along with large-volume bilateral emboli. Interval CT findings indicated evidence of right heart strain, including contrast reflux into the inferior vena cava (IVC), septal straightening and atrial enlargement. Urgent echocardiography was arranged and demonstrated normal left ventricular function, a dilated right ventricle with moderate tricuspid regurgitation, a right ventricular strain pattern and signs of pulmonary hypertension, with a right ventricular systolic pressure of 50mmHg.

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Given these findings, thrombolysis was considered the most suitable treatment option. She received alteplase with a 10mg bolus followed by a 90mg infusion. Table 2 outlines how her oxygen requirement dropped and blood pressure reading improved post thrombolysis. Concurrently, heparin was administered at a rate of 18 units/kg/hour, with regular monitoring of the activated partial thromboplastin time (APTT). Subsequently, the transition was made to enoxaparin sodium at a dosage of 1mg/kg twice daily, leading to the discontinuation of the heparin infusion.

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Remarkably, she exhibited significant improvement over the following days. Her oxygen requirements dropped from 55% to 28% and eventually to room air. Additionally, there was an improvement in her blood pressure, which stabilised at 160/80mmHg. Her blood test results demonstrated notable improvement in the subsequent days, as indicated in Table 1.

Following successful treatment with thrombolysis and initial anticoagulation, she was transitioned to a DOAC, specifically apixaban. Subsequently, she was discharged home with plans for further follow-up at the coagulation clinic to monitor her progress and adjust the treatment regimen as needed.

Discussion

In prior research and clinical applications, the term ‘saddle PE’ has frequently been used interchangeably with ‘massive PE’. However, it is important to clarify that ‘massive PE’ is a haemodynamic designation and should exclusively pertain to a pulmonary embolism presenting with significant haemodynamic compromise. In contrast, patients with saddle PE (SPE) can, and frequently do, exhibit entirely stable haemodynamic indicators and minimal symptoms.

The widespread availability of CT pulmonary angiography (CTPA) has led to an increased recognition of SPE.^11,12,13,14 Regarding clinical presentation, dyspnoea and chest pain were the predominant symptoms, consistent with our observed case. Findings from the PIOPED II study indicated that new-onset dyspnoea at rest or during exertion was the most prevalent symptom among patients with pulmonary embolism in general, especially in those without prior cardiopulmonary disease (73%).¹⁵ Similarly, the EMPEROR study demonstrated that dyspnoea and chest pain were the most frequently reported initial presentations.¹⁶

The acute occurrence of SPE can induce a sudden elevation in pulmonary arterial pressure and pulmonary vascular resistance, resulting in an increased right ventricular (RV) afterload and subsequent RV dilation, ultimately leading to right-heart failure as was evident in this case. The decrease in RV cardiac output also contributes to a reduction in left ventricular (LV) filling, leading to a decline in blood pressure, which may manifest as syncope, hypotension or cardiogenic shock.^5,17 Additionally, acute PE can cause substantial abnormalities in pulmonary gas exchange, leading to hypoxaemia.

Regarding treatment, it has been observed that patients with SPE receive systemic thrombolytic therapy more frequently than the non-saddle PE group.¹⁸ Alkinj B et al found that systemic thrombolysis therapy for late decompensation (occurring > 6 hours after admission) was utilised more often in the saddle PE group compared to the non-saddle PE group (n = 6, 3.2% versus 0%; p = 0.03); similar to this case report.¹⁸ These findings also align with the results of Kwak et al¹⁹ who identified saddle PE as an independent predictor of major adverse events within 30 days of diagnosis. 

Clinicians caring for patients with saddle PE should be vigilant about the possibility of delayed decompensation, and it is recommended to closely monitor clinical and haemodynamic parameters within the initial 12 to 24 hours of admission.

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