History of Present Illness
A 71-year-old woman had been suffering for about 1 month from weakness, daytime sleepiness, loss of appetite with weight loss of 2 kg, low-grade fever (37.8° C [104° F]), diffuse chest pain, exertional dyspnea, and dry cough.
The general practitioner ordered chest radiography, which showed dense opacity in the right upper pulmonary field, and antibiotic therapy (levofloxacin 500 mg daily for 6 days, followed by amoxicillin/clavulanic acid 1000 mg twice a day for 7 days). Because of persisting fever and worsening dyspnea, the patient went to the emergency room.
Past Medical History
The patient was a lifetime nonsmoker. The most significant events in her medical history were arterial hypertension, mild dyslipidemia, and angioplasty with stenting of the left main coronary artery 4 years ago. She was currently under therapy with bisoprolol 1.25 mg/day, ramipril 2.5 mg/day, amlodipine 5 mg/day, acetylsalicylic acid 100 mg/day, and atorvastatin 20 mg/day.
Physical Examination and Early Clinical Findings
Blood tests showed mild leukocytosis (white blood cell [WBC] count 10,130/mm 3 ) and increased inflammatory markers (C-reactive protein [CRP] 66.2 mg/L, normal values < 10 mg/L) and lactate dehydrogenase (LDH; 2359 units/L, normal values < 618 units/L).
Chest radiography confirmed the presence of opacity in the posterior region of the right upper lobe and homolateral basal pleural effusion with fissure involvement ( Fig. 3.1 ).
Clinical Course
The patient underwent chest/abdominal CT before and after administration of contrast medium ( Figs. 3.2 and 3.3 ). The right lung had a reduced volume compared with the contralateral lung. In the dorsal segment of the right upper lobe, there was a solid hyperdense round lesion with irregular margins, about 4 cm in diameter, surrounded by thickened interlobular septa. The mass crossed the major fissure, also involving the apex of the right lower lobe. On the same side, the CT scan showed pleural effusion, with maximum thickness of about 3 cm, and dysventilation of the posterior segment of the right lower lobe. A small pleural effusion (maximum thickness of about 15 mm) was also present on the left side. Several enlarged lymph nodes, with a diameter of about 15 mm, were detected in paratracheal sites. The liver was widely altered by multiple, small, hypodense lesions, some with peripheral enhancement (target or “bull’s eye” lesions).
After obtaining informed consent from the patient, right thoracentesis was performed, resulting in drainage of 500 mL of pleural fluid. Bronchoscopy was scheduled for the next day. However, during the night, the patient experienced severe worsening of dyspnea, and severe hypoxemic respiratory failure occurred. Blood tests showed a rise in WBC (16,830/mm 3 ) and CRP (285.8 mg/L); intravenous antibiotic therapy with imipenem/cilastatin (500/500 mg four times daily) and linezolid (600 mg two times daily) was started. Because of a significant increase in d -dimer (6716 ng/mL), chest CT angiography was performed, and it showed multiple filling defects on the arterial segmental branches in the left upper lobe and the right lower lobe. Hence, a diagnosis of diffuse pulmonary embolism (PE) was made; interestingly, although the right pleural effusion had almost disappeared, a significant amount of left pleural effusion had developed (see Fig. 3.3 ). Echocardiography showed an increase in estimated pulmonary artery systolic pressure (PASP; 40 mm Hg), whereas color Doppler ultrasonography ruled out deep venous thrombosis (DVT) in the lower limbs. Subcutaneous enoxaparin 100 units/kg two times daily was promptly started.
Cytology of the pleural fluid yielded a positive result for cancer cells, and morphology and immune-cytochemical profile were suggestive of pleural involvement by lung adenocarcinoma (tumor cells positive for epithelial cell adhesion molecule [Ber-EP4], thyroid transcription factor 1 [TTF-1], and napsin). However, the low proportion of cancer cells in the pleural effusion did not allow for testing for epidermal growth factor receptor (EGFR) gene abnormalities, anaplastic lymphoma kinase (ALK) rearrangements, or programmed death ligand 1 (PD-L1) expression.
CT of the brain showed several hyperdense round lesions suggestive of cerebral metastases from the lung cancer. Technetium-99m methylene diphosphonate (Tc-99m MDP) bone scintigraphy demonstrated multiple tracer uptakes resulting from widespread metastatic bone disease (skull, sternum, scapulae, ribs, spine, pelvis, left and right humeri, femurs, and fibulae).
