Case Presentation:

A female patient in her late seventies was referred from General Practitioner (GP) to Same Day Emergency Care (SDEC) with right-sided pleuritic chest pain, productive cough, and exertional dyspnoea for the last one week. She has a background of hypertension manages on Ramipril 5 mg once daily. She denies any significant family history of respiratory or cardiovascular diseases. Her symptoms initially manifested as a dry cough; her GP initiated treatment for CAP with oral amoxicillin 500 mg four times daily. However, as the cough progressed to productive and mild right-sided chest pain, clarithromycin 500 mg BD for 5 days was added. However, due to persisting symptoms, a referral to SDEC was made for further evaluation.

During the examination, blood pressure measured 132/80 mmHg, and the heart rate was 75 beats per minute. Right lower base crepitations were detected upon lung auscultation. The Wells score indicated a moderate risk [3], alongside with a D-dimer level of 2210 ng/m. This prompted a CTPA investigation due to ongoing symptoms, heightening suspicion for an undiagnosed PE.

Investigations:
A chest x-ray was obtained, revealing right sided blunting costophrenic angle which may represent infection/pleural effusion (Figure 1). The electrocardiogram (ECG) showed a normal sinus rhythm (Figure 2).  Blood tests, including C-reactive protein (CRP) which is 187 mg/L 0 - 5 and white blood cell count (WBC): 16.3 109/L 4.0 - 10.0, despite having oral amoxicillin 500 mg QDS by the GP for 7 days. Troponin T <13 ng/L. Urea and Electrolytes were normal. The Dimmer test result was 2210 ng/m, indicating high levels. Additionally, a COVID-19 test was conducted, which yielded negative results. Blood cultures and sputum gram stain with culture were negative, as were urinary antigen tests for Streptococcus pneumoniae and Legionella. N-terminal pro B-type natriuretic peptide (NT-pro BNP) and Echocardiogram was normal left ventricular (LV) function and no wall motion abnormalities with normal right ventricular (RV) function size.

Figure 1: CXR: Blunting of the right costophrenic angle which may represent infection/pleural effusion.

Figure 2: 12 leads ECG: Normal Sinus Rhythm.

Given the persistent patient's symptoms despite completing the course of oral antibiotics, and raising D-dimer, a CTPA was performed to rule out PE which demonstrated multiple filling defects in the right lower pulmonary artery and its segmental with subsegmental branches, and patchy consolidations in the right lower lobe with mild right pleural effusion suggestive of infective/inflammatory aetiology ( Figure 3, Figure 4, Figure 5, Figure 6 and Figure 7).

Figure 3: Filling defects in the right pulmonary artery.

Figure 4: Filling defects in the right pulmonary segmental branches.

Figure 5: Filling defects in the right pulmonary subsegmental branches

Figure 6: Filling defects in the right pulmonary subsegmental branches

Figure 7: CTPA lung window shows patchy consolidations in the right lower lobe with mild right pleural effusion suggestive of infective/inflammatory aetiology.

Treatment:
As the PESI score was low risk and the patient is clinically stable. She was discharged with rivaroxaban 15 mg BD for 21 days followed by 20 mg OD for four months [6]. Furthermore, she was treated for CAP with IV ceftriaxone 2 g once daily for 7 days.

Outcome and follow up:

After 7 days of having the above antibiotics, CRP inflammatory markers have improved, and the patient felt well with no chest pain or cough and the breathless is improving. She is doing well on follow up.

Discussion:
Pulmonary embolism (PE) is a common cardiology emergency characterized by the obstruction of a pulmonary vessel due to a dislodged blood clot, typically caused by a thrombus originating from the lower extremity veins which can be acute life threatening. Clinical manifestations include symptoms such as shortness of breath, pleuritic chest pain, coughing, orthopnoea, painful swelling in the calf or thigh, wheezing, haemoptysis, and, less frequently, heart arrhythmia [7]. In more severe cases, it may present with a syncopal attack or, more critically, as circulatory collapse [8]. PE can be diagnosed on CTPA due to its high sensitivity and specificity, revealing a filling defect upon contrast enhancement in the pulmonary artery or any of its branches [9]. However, if CTPA is contraindicated, a ventilation-perfusion (V/Q) scan can be performed. This alternative method shows impaired perfusion with normal ventilation, but it has low sensitivity and specificity [10].

Distinguishing between pneumonia and PE in clinical practice presents significant challenges, potentially resulting in diagnostic delays and subsequent complications, culminating in delayed treatments and serious implications [11]. This complexity is accentuated by various situations, such as infarction pneumonia that happen after PE and the simultaneous occurrence of community-acquired pneumonia (CAP) with underlying PE. In this case study, the PE progressed to pulmonary infarction, leading to infection of the necrotic lung tissue [12]. The rarity of pulmonary infarction following PE is attributed to the dual blood supply of the lung, occurring at a rate of 10% [13]. Recent literature indicates that elderly patients with cardiopulmonary disease are more prone to experiencing secondary pulmonary infarction following a PE because of the poor collateral circulation [14]. Several studies have observed a higher prevalence of infarction in the right lung [15 ,16]. This observation is consistent with the findings in this particular case report. However, the underlying reason for this phenomenon remains unknown.

A heightened index of suspicion is crucial for the early diagnosis of PE and pulmonary infarction, especially in elderly patients with PE risk factors who present symptoms such as cough, pleuritic chest pain, fever, and shortness of breath, along with consolidation on CXR. In such instances, prompt consideration of a CTPA scan is essential to confirm or exclude PE. In this case report, despite the patient receiving a course of oral antibiotics, the sustained consolidation on CXR raises a high suspicion of PE.

The concurrent presence of CAP and PE represents another manifestation of the link between pneumonia and PE [17]. This situation is infrequent and poses a diagnostic challenge due to significant overlap in clinical symptoms, including fever, cough, shortness of breath, and leucocytosis. In a study, chest pain, shortness of breath, haemoptysis, and fever were identified as independent risk factors for PE in patients initially diagnosed with pneumonia [18]. Conversely, emphasis on dyspnoea and/or chest pain in PE, contrasting with fever, chills, and/or cough, was noted in another study [19]. Notably, only 3.3% of patients initially diagnosed with pneumonia in the latter study were later identified as having acute PE. In our case, initial suspicion leaned towards atypical pneumonia; however, the subsequent lack of therapeutic response and additional diagnostics prompted a reconsideration of the diagnosis.

CAP may increase the risk for venous thromboembolism, possibly through a pro-inflammatory, hypercoagulable state contributing to PE development. CAP can mimic PE, leading to delayed diagnosis and treatment [20]. Hence, clinical indicators such as elevated D-dimer levels, haemoptysis, and sudden deterioration of respiratory function or chest pain should prompt suspicion of concomitant PE. In our case report initially, the patient presented with fever, productive cough, right-sided pleuritic chest pain, and severe shortness of breath, the diagnosis of PE was less likely due to the dominance symptoms that suggest a chest infection. However, clinical parameters, including haemoptysis, and worsening right sided chest pain with high D. dimer after the initial improvement, directed the suspicious to concealed PE.

The following four cases evident the diagnostic challenge of differentiating between pneumonia and PE as summaries in Table 1.

The first case involved a patient initially suspected of atypical pneumonia, with symptoms such as cough and fever. Despite initial treatment, further evaluation revealed a massive right-sided PE, highlighting the potential mimicry of pneumonia by PE. The second case, the patient presented with a sudden onset of exertional dyspnoea, a symptom commonly associated with pneumonia. However, subsequent diagnostic imaging disclosed bilateral segmental PE, emphasizing the deceptive similarity in clinical presentation. The third case, presenting with a productive cough, pleuritic chest pain, and haemoptysis, initially led to a pneumonia diagnosis. However, unexpected findings of intraluminal thrombus in the pulmonary arteries during a contrast-enhanced CT chest shifted the diagnosis towards PE. Fourth case involved a patient admitted for degenerative spinal disease, exhibiting fever and breathlessness. Initially treated for community-acquired pneumonia, the persistence of symptoms and subsequent diagnostic imaging, including a CTPA, revealed features consistent with PE, underscoring the challenge of distinguishing between pneumonia and PE. These cases collectively highlight the importance of a nuanced approach to diagnosis when faced with pneumonia-like symptoms, emphasizing the need for a comprehensive evaluation to discern potential underlying pulmonary embolism.

Given the clinical presentation, we propose pneumonia as a provoked risk factor for developing PE in our case report. Recognizing the presence of underlying PE when diagnosing pneumonia holds therapeutic significance, as it necessitates initiation of anticoagulation therapy. Consequently, it is crucial to assess the patients comprehensively and requesting appropriate investigations accordingly to exclude or confirm PE. In conclusion, it is imperative to acknowledge the association between pneumonia and PE and carefully assess and evaluate the clinical and laboratory findings, as well as CXR, when deciding to conduct a CTPA scan for patients developing pneumonia, aiming to promptly identify concealed PE.

Learning points/ Take home messages.    

1. Pneumonia can mimic PE due to symptoms overlap.
2. CAP can develop after infarction pneumonia.
3. PE can be provoked by pneumonia.
4. Worsening symptoms and persistent CXR consolidation in pneumonia may indicate concealed PE.
5. CXR consolidations aren't exclusive to pneumonia; infarction pneumonia is a potential alternative, emphasizing the need for precise diagnosis.