How bad can life be? A case of concurrent cardiac tamponade and pulmonary embolus

Abstract

We present a rare case of a patient presenting with submassive pulmonary embolism (PE) further complicated by cardiac tamponade with the clinical dilemma on whether to perform thrombolysis or emergency pericardiocentesis to save her life. The aetiology of her pericardial effusion remains unclear but may possibly relate to post‐PE pericarditis, a condition that resembles Dressler's syndrome. The pathophysiological processes of concurrent PE and cardiac tamponade combined to result in an unusual right ventricular shape on transthoracic echocardiography, and our findings raise the possibility of a fourth mechanism for the explanation of McConnell's sign – restricted free wall dilation via the moderator band.

Introduction

Concurrent pulmonary embolism (PE) and cardiac tamponade are an extremely rare occurrence, both contributing to a high risk of obstructive cardiogenic shock and death. The acute management of such a case poses a difficult clinical dilemma as they have opposing treatments, each with significant potential consequences. Echocardiography plays a key role in not only diagnosis but also assessment of which life‐threatening disease process should be addressed first.

Case Presentation

A 70‐year‐old woman presented to a regional hospital following a syncope preceded by two days of right shoulder‐tip pain and dyspnoea. On arrival, she was hypoxic, but not hypotensive. Her admission electrocardiograph (ECG) showed widespread T‐wave inversion. Laboratory investigations were normal except for elevated serial troponins with a peak of 0.84 mcg/L. A computer tomography pulmonary angiogram (CTPA) confirmed extensive acute bilateral pulmonary embolus.

A transthoracic echocardiogram (TTE) showed severe right ventricular (RV) dysfunction with severe pulmonary hypertension (RV systolic pressure of 81 mmHg), moderate tricuspid regurgitation and a small left ventricle (LV) with abnormal septal motion consistent with near cavity pressure overload. There was no pericardial effusion. She did not receive thrombolysis as her blood pressure remained normal. She received a stat dose of therapeutic enoxaparin and was subsequently commenced on apixaban.

Apart from travelling to Cambodia over three months prior, there were no other identifiable risk factors for developing PE. She lived alone, worked as a cleaner with good exercise tolerance, was a lifelong non‐smoker, drank minimal alcohol and did not take any regular medications. She had not experienced any constitutional symptoms leading up to her admission.

On the fifth day of admission, she re‐developed right shoulder‐tip pain along with tachycardia and worsening hypoxia, but her blood pressure remained stable. A repeat CTPA showed similar distribution of PE bilaterally but there was now a new mild–moderate pericardial effusion, bilateral moderate pleural effusions and possible right pulmonary infarction (Figure 1). Prior to transfer to our tertiary centre intensive care unit (ICU), she was intubated by the adult retrieval service, which precipitated severe hypotension requiring inotropic support.

Figure 1.

CT Pulmonary Angiogram after deterioration on day 5 demonstrating bilateral PE, new pericardial effusion and bilateral moderate pleural effusions.

On arrival at our ICU, an ECG demonstrated widespread PR depression and inferolateral ST elevation (Figure 2). An urgent bedside TTE showed a large pericardial effusion 25 mm in diameter with a hyperdynamic but under‐filled LV. The right atrium (RA) was enlarged but not collapsing, and the RV was severely dilated from significant septal displacement due to RV overload (Figure 3). The moderator band appeared to divide the RV into an almost akinetic anerusymal mid‐free wall and a vigerously contracting apex. Other features of tamponade, such as mitral and tricuspid inflow variation and inferior vena cava distension, were not formally assessed due to patient instability.

Figure 2.

Electrocardiography on arrival to ICU demonstrating widespread PR depression with reciprocal PR elevation in aVR, in addition to concave upward inferolateral ST elevation without significant reciprocal changes is more suggestive of pericarditis than ischaemia.

Figure 3.

Transthoracic echocardiogram on arrival to ICU demonstrating moderate to large pericardial effusion, dilated right atrium and unusual right ventricular shape with aneurysmal free wall and vigorous contraction at the apex, both separated by the moderator band (atypical McConnell's sign).

Differential diagnoses of the severe shock included further PE with progressive RV failure, cardiac tamponade, or less likely, acute myocardial infarction. Determining the correct diagnosis was crucial because of the opposing treatments of either thrombolysis or pericardiocentesis. The TTE findings were not classic for tamponade but the effusion was clearly large and appeared to have expanded rapidly. The dilated right heart was consistent with the known submassive PE whilst the hyperdynamic and under‐filled LV was felt to be consistent with both conditions. In the limited time available, it was concluded that the new haemodynamic deterioration was most likely due to tamponade and, after administration of two units of fresh frozen plasma, 200 ml of blood stained pericardial fluid was aspirated.

There was immediate improvement in her measured cardiac index and cessation of noradrenaline within 2 h. Her case was discussed with a pulmonary hypertension referral centre who suggested that further intervention for the PE, such as catheter aspiration, was not indicated given the good haemodynamic response and absence of further deterioration. A TTE eighteen days post‐ICU admission showed progressive improvement in RV size and function in addition to her recovering exercise tolerance.

Discussion

There are very few published cases of concurrent pericardial effusion and PE, with the majority of these cases due to underlying malignancy1, 2, 3 or trauma.4 Our case is unique as we have not identified a clear underlying cause for her pericardial effusion. At present no malignancy has been detected on CT imaging, mammography or pericardial fluid. Spontaneous haemopericardium from anticoagulation is a rare occurrence in the non‐trauma setting,5 and apixaban has lower rates in major bleeding when compared with other novel anti‐coagulants and vitamin K antagonists.6

One possible explanation is post‐PE pericarditis, an uncommon complication known to sometimes produce cardiac tamponade.7, 8 This syndrome closely resembles post‐myocardial infarction syndrome, also known as Dressler's syndrome, and responds well to anti‐inflammatory therapy such as glucocorticoids.9 The widespread PR depression with reciprocal PR elevation in aVR in addition to the concave upward ST elevation without significant reciprocal ST depression were, in retrospect, highly suggestive of underlying pericarditis.

There are two proposed pathophysiological mechanisms for post‐PE pericarditis, the first of which is a poorly understood immunological process whereby pulmonary infarction results in a hypersensitivity reaction leading to pericardial inflammation. The second mechanism is due to direct contiguity of pleura and pericardium.8, 10 Our patient's pulmonary infarction may have led to inflammation of adjacent pleura and consequently the parietal pericardium.

The TTE findings are fascinating due to the concurrent presence of two pathophysiological processes. Acute PE can cause RV distension and dysfunction due to pulmonary outflow tract obstruction. Cardiac tamponade, on the other hand, can restrict RV distension due raised intra‐pericardial pressure. Indeed, chamber compression is one of the earliest echocardiographic findings of cardiac tamponade, with the right‐sided chambers being most vulnerable due to their lower intra‐cardiac pressure.11 In our patient, the combination of pathophysiological forces meant that not only did the right‐sided chambers not collapse, but in addition the RV took an unusual shape with an aneurysmal free wall and vigorous contraction at the apex, both separated by the moderator band – an atypical McConnell's sign.

Although echocardiography has poor sensitivity for acute PE, the presence of McConnell's sign is considered highly specific.12 It is a pattern of regional RV dysfunction with akinesia of the mid‐free wall but normal motion at the apex. There are currently three mechanisms proposed to explain the sign – (a) tethering of the RV apex to a contracting and often hyperdynamic LV may account for the preserved apex motion; (b) the RV may be assuming a more spherical shape to equalise regional wall stress; and (c) localised ischaemia of the RV free wall due to increased wall stress.13, 14 Our TTE findings raise the possibility of a fourth mechanism for the explanation of McConnell's sign – restricted free wall dilation via the moderator band.

Conclusion

Although rare, cardiac tamponade should be considered early in shocked patients with pulmonary embolism due to their opposing treatments. Our patient's presentation remains idiopathic but may relate to post‐PE pericarditis, a condition that closely resembles Dressler's syndrome. Emergency pericardiocentesis dramatically improved her clinical shock by relieving one of the contributory factors of her restricted LV filling. The opposing pathophysiological processes of PE and tamponade combined to display fascinating echocardiography images. In particular, our TTE findings raise the possibility of a fourth mechanism for the explanation of McConnell's sign – restricted free wall dilation via the moderator band.

Authorship declaration

The authors conform with the journal's authorship policy and are in agreement with the content of the submitted manuscript.

Funding

No funding information is provided.

Disclosure statement

None declared.

Supporting information

Video S1 QuickTime video file of TTE on arrival to ICU (as per Figure 3).