A 69-year old woman, previous smoker (30 pack years (PY)) presented with dry cough, headache, dyspnoea at rest and general malaise. The symptoms appeared 21/2 weeks prior to admission, and. Six days treatment with antibiotics and corticosteroids did not have any effect. Before admission, the patient had never experienced pulmonary symptoms. At admission, the patient had a temperature of 39.5  C, normal blood pressure, saturation of 92% and basal crackles at lung auscultation. Blood samples showed a mild anaemia, elevated C-reactive protein 174.5 mg/ml (CRP) and normal leucocytes (LKC). No deep venous thromboembolism was present on clinical examination. Echocardiography showed a normal left ventricular ejection fraction of 60%, a borderline dilated and hypertrophic left ventricle and no signs indicating increased pulmonary pressure. Tests for atypical pneumonia, tuberculosis and fungal infections were negative.
Intravenous broad-spectrum antibiotics were initiated but due to continuing fever and an elevated CRP, a chest X-ray and an HRCT were performed. On the chest radiograph, blurry bilateral less than 1 cm large consolidations were present predominantly on the left side.
HRCT revealed diffuse ground glass opacities, thickening of interlobular septae, traction bronchiectasis, localized subpleural honeycombing, mosaic perfusion pattern in the apical areas of the lung parenchyma and mediastinal lymphadenopathy. Radiologically, a diagnosis of pulmonary fibrosis and infection was made (Fig. 1A and 1B). CT angiography did not demonstrate pulmonary embolisms. Chronic eosinophilic pneumonia (CEP) or fibrotic non-specific interstitial pneumonia (NSIP) was suggested as an underlying interstitial lung disease with simultaneous infection.
Prophylactic low-molecular-weight-heparin was administered together with oxygen, intermittent continuous positive airway pressure (CPAP) and high dose corticosteroid. Despite treatment, the patient's condition deteriorated and respiratory support including high frequency oscillation and NO treatment was started at the intensive care unit, where, as a consequence of multi-organ failure, she succumbed after 21 days of hospitalisation.
A post mortem autopsy showed widespread pulmonary infarction of different age with haemorrhagic necrosis. There were limited areas with signs of previous infection, and diffuse extensive emphysema, but no fibrosis. The cause of death was determined to be caused by haemorrhagic pulmonary infarction, caused by widespread bilateral pulmonary thrombosis.