What is the most likely mechanism in a young woman on prednisone (corticosteroid) presenting with fever, pleuritic chest pain, and dyspnea, with a computed tomography (CT) scan showing a segmental pulmonary artery defect?

Mechanism of Pulmonary Artery Defect in Young Woman on Prednisone

The most likely mechanism is thromboembolism causing pulmonary embolism, with corticosteroid therapy (prednisone) serving as a significant prothrombotic risk factor that increases venous thromboembolism risk through multiple pathways including hypercoagulability and endothelial dysfunction.

Clinical Presentation Analysis

This patient presents with the classic triad highly suggestive of pulmonary embolism:

• Fever is present in approximately 7% of PE cases 1
• Pleuritic chest pain occurs in 52% of PE cases, typically caused by pleural irritation from distal emboli 1, 2
• Dyspnea is the most common symptom, present in approximately 80% of PE patients 1
• CT showing segmental pulmonary artery defect is diagnostic of pulmonary embolism 1

The British Thoracic Society guidelines emphasize that the combination of tachypnea (>20/min), pleuritic pain, and arterial hypoxemia strongly suggests PE, and the absence of all three virtually excludes the diagnosis 3.

Corticosteroid-Induced Hypercoagulability

Prednisone is a well-established risk factor for venous thromboembolism through several mechanisms:

• Corticosteroids induce a hypercoagulable state by increasing clotting factors and promoting endothelial dysfunction
• The case literature documents PE occurring in young patients on corticosteroid therapy, particularly in the context of autoimmune conditions like lupus 4
• Predisposing factors are found in 80-90% of PE patients, with medical illness and medications being common contributors 3

Differential Considerations

While the presentation could theoretically suggest other mechanisms, the evidence strongly favors thromboembolism:

Septic embolism is less likely because:

• Septic PE typically presents with more prominent systemic infection signs and bacteremia (85% with S. aureus) 5
• Sources include skin/soft tissue infections (44%), endocarditis (27%), or infected DVT (17%) 5
• This patient lacks clear evidence of these peripheral infection sources

In situ pulmonary artery thrombosis is rare and typically occurs with:

• Underlying pulmonary hypertension
• Malignancy
• Antiphospholipid syndrome 4

Clinical Algorithm for Confirmation

Immediate diagnostic steps should include:

1. Assess clinical probability using risk factors (corticosteroid use qualifies as medical illness risk factor) 3, 6
2. Obtain D-dimer if not already done - normal levels exclude PE in appropriate clinical contexts 3
3. Lower extremity venous ultrasound - recommended as first-line investigation in patients with suspected PE, especially with prior risk factors 3, 6
4. CT pulmonary angiography confirms the diagnosis and characterizes embolic burden 1

Important Clinical Pitfalls

• Do not dismiss PE based on fever alone - while fever is less common (7% of cases), it can occur and may lead to misdiagnosis as pneumonia 1, 7, 8, 9
• Do not assume pneumonia - PE frequently masquerades as pneumonia, particularly when fever is prominent 7, 8
• Young age does not exclude PE - young women on medications like corticosteroids remain at risk despite age 3
• Normal oxygen saturation does not rule out PE - up to 20-40% of PE patients have normal arterial oxygen pressure 1

Management Implications

Anticoagulation should be initiated immediately based on high clinical suspicion before diagnostic confirmation is complete 3, 6. The British Thoracic Society recommends starting heparin on the basis of high or intermediate clinical suspicion before the diagnosis is clarified 3.