A 42-year-old female presented with worsening cough and breathlessness of two weeks duration. She had past history of internal jugular vein thrombosis and left upper limb deep vein thrombosis. She was a known hypertensive on medication. She was afebrile at the time of examination. Laboratory investigations revealed mild leukocytosis and thrombocytosis with mildly raised D-dimer and positive Lupus anticoagulant. Echocardiography showed mild left ventricular hypertrophy with an ejection fraction of 60%.
Chest radiograph revealed multiple nodular opacities in both lungs, few showing internal lucency, suggestive of cavitation. There was left moderate and right minimal pleural effusion with mild cardiomegaly. No peripheral or central venous line was noted. Left-sided effusion was drained with an intercostal drainage tube. A computed tomography (CT) pulmonary angiography of chest was performed. Multiple well-defined, thick-walled, cavitating and non-cavitating nodules were seen in both lungs. They did not contain air-fluid levels or enhancing soft tissue component. Bilateral pleural effusion was present. There were no features of pulmonary hypertension or thrombosis. Mediastinal and left axillary lymphadenopathy was present. There was vascular engorgement over the left anterior chest, due to collaterals formed as a result of previous left upper limb deep vein thrombosis.
The possibility of septic emboli was considered and bronchoalveolar lavage was performed, which tested positive for Citrobacter. Intravenous antibiotics were started and the patient showed clinical improvement. Anti-neutrophil cytoplasmic antibody tests for c-ANCA and p-ANCA were negative. A CT- guided biopsy was planned to confirm the diagnosis. This revealed necroinflammatory tissue with neutrophils. There was no evidence of vasculitis or neoplasm.
A cavity is defined as a lucency within a pulmonary consolidation, mass or nodule. A combined analysis of symptoms, previous clinical history, laboratory and imaging findings is necessary to reach a diagnosis. The causes of cavitatory lesions broadly include infection, systemic diseases, neoplasm and miscellaneous causes .
Septic emboli are usually seen in patients with infective endocarditis, indwelling catheters and a source of sepsis such as periodontal disease or deep vein thrombosis. The most frequently associated organism is Staphylococcus . Clinical history can reflect rapid clinical deterioration and elevated lymphocyte counts. Imaging features include cavitating or non-cavitating nodules or peripheral wedge shape consolidations. A ‘feeding vessel’ sign which represents a pulmonary arterial branch coursing to the centre of the nodule may be seen. This was earlier considered to be highly specific to the condition ; however, it may be seen in other diseases such as angioinvasive pulmonary aspergillosis, pulmonary embolism, arteriovenous malformation and metastasis. Another differential is Wegener’s granulomatosis, a multisystem vasculitis affecting respiratory system, kidneys and skin. Most patients have an elevated c-ANCA level. On imaging, a ‘halo sign’ may be seen due to haemorrhage, which is represented by ground-glass opacity surrounding a nodule . Cavitating metastasis is another differential to be considered. A primary should be excluded. Metastases from squamous cell carcinoma, adenocarcinoma or sarcomas tend to cavitate. Spontaneous pneumothorax can occur in case of osteosarcoma metastases .
In any suspected infection, other features should be looked for, such as consolidation with air bronchograms, ‘split pleura sign’ (empyema), ‘bulging fissure sign’ (Klebsiella pneumonia), tree in bud pattern nodules, air-fluid level in a cavity (abscess), halo and reverse halo signs (fungal infection) and water-lily sign (Hydatid cyst) . The management in a case of septic emboli includes treating the source of infection such as drainage of abscess, removal or replacement of an infected catheter and antibiotic treatment.
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