In an adult presenting with acute pleuritic chest pain, dry or blood‑tinged cough, possible hemoptysis, and risk factors for thromboembolism, what are the typical clinical features, diagnostic work‑up, and treatment for pulmonary infarction?

Pulmonary Infarction: Clinical Presentation, Diagnosis, and Management

In an adult presenting with acute pleuritic chest pain, dry or blood-tinged cough, possible hemoptysis, and risk factors for thromboembolism, pulmonary infarction should be suspected as a manifestation of pulmonary embolism, requiring immediate risk stratification, D-dimer testing (if low-to-intermediate probability), CT pulmonary angiography for confirmation, and anticoagulation as the cornerstone of treatment. 1

Clinical Presentation

Cardinal Symptoms

Pulmonary infarction presents with a characteristic symptom complex:

• Pleuritic chest pain is the dominant symptom, occurring in approximately 52-75% of patients with pulmonary infarction, caused by pleural irritation from distal emboli producing alveolar hemorrhage 1, 2, 3
• The pain is sharp, stabbing, or burning in quality and intensifies with deep breathing, coughing, or other respiratory movements 2, 3
• Dyspnea is present in 72-82% of PE cases and may be the sole presenting symptom in patients with pre-existing heart failure or chronic lung disease 1, 4
• Hemoptysis occurs in 5-11% of cases and frequently accompanies pleuritic chest pain and alveolar hemorrhage 4
• Cough (dry or blood-tinged) is reported in approximately 20% of pulmonary embolism patients 1, 4

Physical Examination Findings

• Tachypnea (respiratory rate >20/min) occurs in approximately 70% of PE patients 1, 4
• Tachycardia is present in over 90% of cases 4
• The combination of dyspnea, tachypnea, or pleuritic pain is present in 97% of PE patients; only 3% lack all three features 1, 2, 4
• Clinical signs of deep vein thrombosis (leg swelling) are evident in only 10-15% of patients 4

Critical Diagnostic Pitfalls

• Nearly 48% of PE patients do not experience any chest pain, so absence of pain does not exclude pulmonary infarction 2, 4
• Between 20-40% of PE patients have normal arterial oxygen saturation 1, 2, 4
• Individual clinical features have predictive value less than 80%; no single sign or symptom can reliably diagnose or exclude PE 1, 4

Risk Factors for Thromboembolism

Assess for the following predisposing factors, as PE probability rises with the number present 4:

• Immobilization within the past 4 weeks 3
• History of prior DVT or PE 3
• Active malignancy 3
• Recent surgery (especially orthopedic or abdominal) 1, 3
• Prolonged travel 3
• Oral contraceptive use in young women 1
• In 30-40% of cases, no identifiable risk factor is present (unprovoked PE) 4

Diagnostic Work-Up

Step 1: Clinical Probability Assessment

Apply validated clinical decision rules to estimate pre-test probability:

• Use either the Wells score or revised Geneva score to categorize patients as low, intermediate, or high probability (or PE-unlikely vs. PE-likely in two-tier systems) 1, 3
• The proportion of confirmed PE is approximately 10% in low-probability, 30% in moderate-probability, and 65% in high-probability categories 1

Step 2: D-Dimer Testing

• In patients with low-to-intermediate clinical probability, obtain an age- and sex-adjusted D-dimer test 3
• A negative D-dimer safely excludes PE in low-to-intermediate probability patients 1, 3
• D-dimer has high negative predictive value but poor specificity; elevated levels occur with cancer, inflammation, bleeding, trauma, surgery, and necrosis 1
• Do not order D-dimer in high-probability patients; proceed directly to imaging 1

Step 3: Imaging Studies

CT Pulmonary Angiography (CTPA):

• CTPA is the definitive diagnostic test for pulmonary embolism and infarction 1, 3
• Pulmonary infarcts appear as peripheral, pleural-based consolidations with a convex margin toward the hilum, casting a semicircular or cushion-like density 5, 6
• The classic wedge-shaped appearance is seen in only 44% of cases; the apical portion is typically spared due to collateral blood flow 5, 6
• Focal areas of hyperlucency within the infarction are often visible on CT 5
• Pleural effusion develops in approximately 46% of PE cases and is frequently hemorrhagic 3, 4

Chest Radiography:

• Chest X-ray is frequently abnormal but findings are non-specific (atelectasis, pleural effusion, elevated hemidiaphragm) 1, 4
• Its main value is excluding alternative diagnoses such as pneumothorax, pneumonia, or lobar collapse 1

Electrocardiography:

• ECG changes suggestive of myocardial ischemia occur in 71% of PE patients 7
• Common findings include inverted T waves in V1-V4, S1Q3T3 pattern, QR pattern in V1, and right bundle branch block 4, 7
• ST-segment depression in V4-V6 and ST-segment elevation in V1 and aVR are significantly more common in high-risk PE 7
• One-third of PE patients may present with chest pain, elevated troponin, and ECG changes mimicking acute coronary syndrome 7

Step 4: Risk Stratification

Classify PE severity based on hemodynamic status and markers of right ventricular dysfunction 1:

High-Risk PE (early mortality >15%):

• Presence of shock or persistent hypotension (systolic BP <90 mmHg for ≥15 minutes) 1, 4
• Indicates central or extensive embolic burden with severely reduced hemodynamic reserve 1, 4

Intermediate-Risk PE (mortality 3-15%):

• At least one marker of RV dysfunction (RV strain on ECG, elevated cardiac biomarkers, RV dilation on echocardiography) 4
• May present with syncope, which occurs in 14-19% of PE cases 4

Low-Risk PE (mortality <1%):

• No evidence of RV dysfunction or myocardial injury 4
• Typically presents with isolated, mild symptoms 4

Treatment

Anticoagulation: The Cornerstone of Therapy

Immediate anticoagulation is the standard treatment for pulmonary infarction:

• Begin anticoagulation as soon as PE is confirmed (or strongly suspected while awaiting confirmation in high-probability patients) 1, 8
• Options include low-molecular-weight heparin, unfractionated heparin, fondaparinux, or direct oral anticoagulants 1
• Anticoagulation prevents recurrent embolism; death from recurrent PE after adequate anticoagulation is exceptional 1

Thrombolytic Therapy

Systemic thrombolysis is indicated for high-risk PE with hemodynamic instability:

• Thrombolytic treatment provides rapid clot resolution in patients with shock or persistent hypotension 1, 4, 8
• Consider surgical embolectomy or catheter-directed therapy if thrombolysis is contraindicated or fails 1, 4

Special Clinical Scenarios

Young patients with isolated pleuritic chest pain:

• In patients aged <40 years with isolated pleuritic pain, no risk factors for thromboembolism, respiratory rate <20/min, and normal chest radiograph, PE is very unlikely 1
• Avoid unnecessary admission and empiric anticoagulation in this low-risk group 1

Post-operative patients:

• PE is often confused with segmental/lobar collapse or infection after upper abdominal surgery 1
• Relative contraindications to anticoagulation may exist; carefully weigh risks and benefits 1

Prognosis and Follow-Up

• The PIOPED study found that 25% of anticoagulated PE patients died within one year, with almost half dying within two weeks 1
• Most deaths were due to underlying disease rather than recurrent embolism 1
• Many patients were already hospitalized before PE occurred, and the prognosis of the underlying disease may be more serious than the thromboembolism itself 1