An unusual presentation of pulmonary embolism

Abstract

Pulmonary embolism (PE) is a common cardiovascular emergency, by which occlusion of a part of the pulmonary arterial bed may lead to acute life threatening but potentially reversible right ventricular failure. Early diagnosis is fundamental to implement immediate effective treatment to reduce mortality. However, the diagnosis can be easily missed due to non-specific clinical presentation. We wish to present an unusual case whereby a patient with no risk factors for PE, symptoms suggestive of acute pericarditis and an ECG showing concave ST segment elevation was found to have multiple pulmonary emboli.

Background

Pulmonary embolism (PE) occurs as a complication of venous thrombosis. The risk factors for venous thrombosis include endothelial injury, hypercoagulability of blood and stasis.^{1 2} Evaluating the likelihood of PE in a patient according to their clinical presentation is most important when selecting appropriate diagnostic tests and interpreting the significance of their results.^{3 4} In the majority of cases, PE presents with symptoms such as pleuritic chest pain, shortness of breath, haemoptysis and syncope. Typical clinical signs include tachycardia, tachypnoea, hypoxia and cyanosis.^{1 3} ECG findings associated with PE are variable and range from the classical S_I Q_III T_III pattern to non-specific changes such as sinus tachycardia and signs of right ventricular strain.^{3 5 6} ST segment elevation mimicking the ECG pattern produced with an anteroseptal myocardial infarction is a rare but previously reported manifestation of PE;⁷ however, the occurrence of concave ST segment elevation is not a recognised feature of PE. This case illustrates that rare manifestations of common pathology can often be challenging to diagnose especially when both symptoms and investigation findings are the classical features of a completely different condition.

Case presentation

A 63-year-old woman presented to the cardiology department with a 1-day history of central chest pain and recent antibiotic treatment for a productive cough. The pain was described as tightness in the chest exacerbated on deep inspiration and on lying down in a supine position and relieved on sitting up and leaning forwards. She had a body mass index of 25, never smoked and led an active lifestyle. She had a background of asthma but was otherwise fit and well with no history of malignancy, venous thromboembolism, surgery or hormone-replacement therapy. There was also no history of shortness of breath or any recent foreign or long-distance travel. On examination she was apyrexial and her blood pressure and heart rate were 105/65 mm Hg and 75 beats/min, respectively. Her jugular venous pressure was measured at 2 cm above the sternal angle and heart sounds were normal, with no added sounds. Her respiratory rate was 16/min and oxygen saturations were 98% on air. Her chest was clinically clear on auscultation and chest x-ray showed evidence of a small left pleural effusion with mild pulmonary congestion. Initial blood results revealed elevated inflammatory markers with a white cell count of 13 × 10⁹/litre and neutrophil count of 9 × 10⁹/litre, C reactive protein of 106 mg/l and erythrocyte sedimentation rate of 17 mm/h. Her estimated creatinine clearance was 83.9 ml/min. ECG showed progressive concave ST elevation in the anterior leads (figures 1 and 2). Based on the history and the results of the diagnostic tests, a diagnosis of pericarditis was suspected and she was planned for discharge the next morning with anti-inflammatory medication.

Figure 1.

Initial ECG showing concave ST segment elevation in the anterior leads.

Figure 2.

Repeat ECG 40 min later showing progressive concave ST segment elevation in the anterior leads.

The following morning, she was symptom-free but was found to have fluctuating oxygen saturations between 92% and 98%. Subsequent arterial blood gas testing on air revealed a PO₂ of 9.29 kPa, PCO₂ of 5.43 kPa, HCO₃⁻ of 20.1 mmol/l, lactate level of 1.7 mmol/l, pH of 7.315 and anion gap of 12.1 mmol/l. Her Well's score was calculated and being −3, indicated a low probability of PE. However, a D-dimer assay was taken and found to be raised at 1003. Hence, CT pulmonary angiography (CTPA) was carried out and showed confirmatory evidence of acute multiple right-sided pulmonary emboli (figure 3).

Figure 3.

CT pulmonary angiography demonstrating multiple right-sided pulmonary emboli.

Outcome and follow-up

She was started on anticoagulant therapy with warfarin and discharged a few days later following resolution of her symptoms.

Discussion

It is well recognised that a careful assessment based on good history, clinical examination and use of simple tests such as an ECG, chest x-ray and arterial blood gas sampling play a significant role in identifying the risk of PE in patients presenting with chest pain.⁸

The electrocardiographic findings associated with PE have been well described in the medical literature for over 50 years, and these features include changes in rhythm, axis and morphology of the QRS complexes and T waves.⁹ It has been suggested that typical abnormalities include (a) an S_I Q _III or S_I Q _III T_III pattern, (b) rightward QRS axis shift, (c) transient, complete or incomplete RBBB, (d) T wave inversion in the right precordial leads and (e) sinus tachycardia.¹⁰ Findings of ST segment elevation in the precordial leads mimicking an anterior myocardial infarction, although uncommon, have been previously reported.¹¹

The chest radiograph is generally non-diagnostic, although it is useful for excluding alternative diagnoses¹² such as pneumonia or pneumothorax.

Echocardiography is generally not recommended as a routine imaging test in the diagnosis of PE although it can be particularly helpful in emergency management decisions when the patient is haemodynamically compromised.³ As the patient in our case was systemically well with no clinical signs of right ventricular overload or dysfunction, echocardiography was not performed.

In our case, there were several factors relating to the patient's presentation that on initial assessment, were inconsistent with the typical features of PE and instead mimicking a diagnosis of pericarditis. This included a lack of risk factors for PE as well as the nature and onset of the pain, which was preceded by a recent productive cough and described as tightness worse when lying flat and better when sitting up and leaning forwards. This was followed by radiological findings on the chest x-ray consistent with a lower respiratory tract infection. There was also a lack of dyspnoea, tachypnoea and tachycardia throughout the admission, which tends to be unusual with PE.¹³ The most interesting and unique abnormality was the progressive concave ST segment elevation in the precordial leads, which is a classical electrocardiographic feature of pericarditis^{14 15} and has not been previously associated with PE. However, the metabolic acidosis revealed in the arterial blood gas analysis was of unknown origin and may have temporarily contributed to temporary alterations of the electrographic patterns. The only findings that raised suspicion towards an alternative diagnosis were the intermittent fluctuation of oxygen saturations down to 92% and arterial PO₂ of 9.29 kPa in room air, both of which in the context of her background of asthma, could be of questionable significance. Fortunately, these results were not dismissed and she was further investigated to reach the correct diagnosis.

Learning points.

• In pulmonary embolism (PE) concave ST segment elevation is rare, and this case demonstrates how a patient with a PE can present with misleading features mimicking those of pericarditis.

• Physicians should maintain a high level of suspicion of PE even when complaints and signs are neither suggestive nor specific.

• Diagnosis of PE is often based on a systematic approach, which should be triggered when there are suggestive or unresolved symptoms or signs as the potential consequences of missed diagnosis could be catastrophic.

• PE continues to present a diagnostic challenge for the clinician and good clinical judgement combined with appropriate investigations can help reduce mortality from this condition.