Pulmonary Embolism and Pneumonia: Clinical Factors to Consider

Pulmonary embolism (PE) and pneumonia are serious conditions with overlapping symptoms, making diagnosis challenging. Both can cause shortness of breath, chest pain, and fever, but they require different treatments, making accurate differentiation essential.

Pulmonary Embolism Clinical Presentation

Pulmonary embolism presents with a range of symptoms, from mild discomfort to sudden cardiovascular collapse. Dyspnea is the most common symptom, occurring in about 73% of cases, according to The Lancet. This shortness of breath develops rapidly and is typically unrelated to exertion, distinguishing it from other respiratory conditions. Patients often describe a sensation of air hunger or an inability to take a full breath.

Chest pain, reported in approximately 44% of cases, varies based on the location of the embolism. Pleuritic pain—sharp and worsened by deep inspiration—suggests peripheral pulmonary vasculature involvement, while a more central embolism may cause a dull, pressure-like discomfort resembling angina. This distinction helps differentiate PE from conditions like myocardial infarction.

Hemodynamic instability, particularly in massive PE (5% of cases), signals significant obstruction of the pulmonary circulation. Hypotension—systolic blood pressure below 90 mmHg or a drop of at least 40 mmHg for more than 15 minutes—can lead to obstructive shock, resulting in systemic hypoperfusion. Signs such as altered mental status, cold extremities, and oliguria indicate worsening circulatory failure, which can progress to cardiogenic shock without immediate intervention.

Tachycardia, seen in up to 30% of patients, often exceeds 100 beats per minute as a compensatory response to impaired oxygenation. While sinus tachycardia is the most frequent electrocardiographic abnormality, the S1Q3T3 pattern may suggest right heart strain. However, these ECG changes lack specificity and should be considered alongside clinical suspicion and imaging findings.

Atypical presentations are more common in elderly patients or those with comorbidities. Syncope, occurring in about 10% of cases, often indicates a large clot burden or significant hemodynamic compromise. Isolated hypoxemia without obvious respiratory distress can be an early clue, especially in the absence of chronic lung disease. Low-grade fever may also be present, complicating differentiation from infectious causes.

Pneumonia Clinical Presentation

Pneumonia symptoms vary based on the infectious agent, host immune status, and severity of lung involvement. The most common initial complaint is cough, which may be productive or dry. Bacterial pneumonia, particularly from Streptococcus pneumoniae, often presents with a sudden onset of high fever, chills, and purulent sputum production. In contrast, atypical pneumonia, associated with Mycoplasma pneumoniae or viral pathogens, develops gradually with a persistent dry cough and milder fever.

Shortness of breath is a prominent feature, especially in cases with extensive alveolar consolidation. Patients may experience progressive breathlessness, worsening with exertion or even at rest in severe cases. Hypoxemia can develop if large portions of the lung parenchyma are affected, leading to increased respiratory effort. In elderly individuals or those with preexisting pulmonary disease, pneumonia may present with subtle signs such as confusion or fatigue, delaying diagnosis.

Chest discomfort is frequently reported, particularly when the infection extends to the pleura. Pleuritic pain—sharp and exacerbated by deep breathing or coughing—suggests pleural involvement, commonly seen in bacterial pneumonia. Unlike myocardial ischemia, pleuritic pain is localized and often accompanied by splinting, where patients instinctively limit chest expansion to reduce discomfort. Parapneumonic effusion can further exacerbate dyspnea and dullness to percussion.

Systemic manifestations such as fever, chills, and malaise reflect the body’s inflammatory response. Fever patterns may provide diagnostic clues, with bacterial pneumonia typically causing high, spiking fevers, while viral pneumonia results in lower-grade temperature elevations. Night sweats and myalgias can accompany both bacterial and atypical infections. In immunocompromised individuals, fever may be absent despite significant pulmonary involvement, emphasizing the need for a comprehensive clinical assessment.

Risk Factors for Both Conditions

Several factors increase susceptibility to both pulmonary embolism and pneumonia, complicating diagnosis. Hospitalization is a major contributor, as prolonged immobility promotes venous stasis, predisposing individuals to deep vein thrombosis (DVT) and subsequent PE. Simultaneously, exposure to nosocomial pathogens and mechanical ventilation increases the risk of pneumonia, particularly ventilator-associated pneumonia (VAP), which has a high mortality rate.

Chronic cardiopulmonary diseases further blur the clinical picture. Chronic obstructive pulmonary disease (COPD) exacerbations, often triggered by infections, can mimic pneumonia or coexist with it. Meanwhile, COPD-related endothelial dysfunction and systemic inflammation contribute to a hypercoagulable state, increasing PE risk. A study in Chest found that COPD patients have double the risk of PE compared to the general population. Similarly, heart failure can cause pulmonary congestion that may resemble pneumonia, highlighting the need for careful diagnostic evaluation.

Cancer and its treatments add complexity. Malignancies, particularly lung, pancreatic, and gastrointestinal cancers, are associated with a hypercoagulable state, increasing PE risk. Chemotherapy and radiation therapy further elevate clotting risk while weakening immune defenses, making infections more severe. Studies indicate cancer patients are up to seven times more likely to develop PE, while also being more vulnerable to pneumonia due to neutropenia and mucosal damage.

Diagnostic Methods

Distinguishing between pulmonary embolism and pneumonia requires a systematic approach integrating clinical assessment with targeted diagnostic testing. A thorough history and physical examination help refine the differential diagnosis. While both conditions can present with dyspnea and chest pain, historical clues—such as recent surgery, prolonged immobility, or known infection exposure—help guide evaluation. Auscultation findings provide further insight; localized crackles or bronchial breath sounds suggest alveolar consolidation in pneumonia, whereas clear lungs with tachypnea raise suspicion for PE.

Imaging plays a central role in confirming the diagnosis. Chest radiography, the first-line modality, can quickly identify pneumonia-related infiltrates but has limited sensitivity for PE. When PE is suspected, computed tomography pulmonary angiography (CTPA) is the preferred test, offering detailed visualization of pulmonary artery thrombi. A Radiology meta-analysis reported CTPA has a sensitivity of 83% and specificity of 96%, making it the gold standard for PE diagnosis. Pneumonia, in contrast, is better characterized by lobar consolidation, air bronchograms, and interstitial opacities, which are more evident on CT when plain radiographs are inconclusive.

Laboratory tests further refine diagnostic certainty. In suspected PE, D-dimer testing is useful for ruling out the condition in low-risk patients due to its high negative predictive value. However, elevated levels are nonspecific and can be seen in infections, malignancy, and recent surgery. For pneumonia, biomarkers such as C-reactive protein (CRP) and procalcitonin help differentiate bacterial from viral etiologies, with procalcitonin levels above 0.5 ng/mL suggesting bacterial infection. Blood cultures and sputum analysis may be necessary in severe cases to identify pathogens and guide treatment.

Potential Complications in Coexisting Cases

When pulmonary embolism and pneumonia occur together, management becomes more complex due to overlapping effects that worsen respiratory and circulatory function. The combined impact of pneumonia-induced inflammation and vascular obstruction from PE can lead to severe hypoxemia. In pneumonia, alveolar consolidation reduces gas diffusion, while PE disrupts pulmonary perfusion, creating ventilation-perfusion mismatch. Patients with preexisting cardiopulmonary disease are particularly vulnerable to respiratory failure requiring mechanical ventilation.

Coexisting pneumonia and PE also increase the risk of systemic complications, including sepsis and hemodynamic instability. The inflammatory response from pneumonia can induce a prothrombotic state, worsening clot burden in PE patients. Conversely, anticoagulation therapy for PE raises the risk of hemorrhagic complications, particularly in bacterial pneumonia with necrotizing infections or cavitary lesions. Clinicians must carefully balance anticoagulation intensity, considering both thrombotic and bleeding risks while ensuring adequate antimicrobial coverage to control infection. In critically ill patients, close hemodynamic monitoring is essential, as worsening septic shock or right ventricular failure can rapidly lead to multi-organ dysfunction, requiring aggressive supportive measures.