A 30-year-old man, who one month before admission presented with cough, headache and progressive dyspnoea on exertion. Two weeks later the patient presented with mucopurulent expectoration and fever of 38ºC. He consulted his doctor who prescribed treatment with amoxicillin and later moxifloxacin and tiotropium bromide. He consulted the emergency department for dyspnoea at rest, severe retrosternal pain and palpitations.
He was a non-smoker and had a history of bronchial asthma, which he treated with inhaled salbutamol.
On physical examination he presented with A.T.: 110/70 mmHg, 37.5º C, he was conscious, tachypnoeic, sweating, with no jugular ingurgitation. Pulmonary auscultation showed diffuse bilateral crackles and cardiac auscultation showed rhythmic, rapid tones without murmurs or extratonos. The abdomen was soft and depressible with no organomegaly. There was no oedema in the extremities and peripheral pulses were preserved.
Laboratory tests showed 18,500 leukocytes with left shift, haemoglobin 16.3 grams/dl, 474,000 platelets, prothrombin activity 73%. D-dimer 920 mg/dl. Baseline arterial blood gases: pH 7.53, pO2 47 mmHg, pCO2 23 mmHg, CO3H 19.2 mmol/l. Normal biochemistry including troponin and CPK.
Chest X-ray showed severe cardiomegaly and a bilateral interstitial pattern. In view of these findings, a transthoracic echocardiogram was performed showing severe pericardial effusion, with no evidence of tamponade and a left ventricle of normal dimensions.
Admission to the intensive care unit, with treatment with furosemide, levofloxacin, acetylsalicylic acid and non-invasive mechanical ventilation.
A new echocardiogram showed signs of tamponade, so a pericardiocentesis was performed, obtaining one litre of serohaematic fluid, with the following biochemical characteristics: LDH 2353 U/l, protein 5.3 gr, 9855 cells with 98% polymorphonuclear.
Seven days later, he was transferred to the Internal Medicine Department where the study to determine the aetiology of the pericardial effusion and the interstitial pattern was initiated, and the following tests were performed: antinuclear antibodies, rheumatoid factor, Mantoux, negative. The thyroid profile was normal.
Pericardial fluid culture was negative, as were three blood cultures.
Pathological anatomy of the pericardial fluid was reported as intense acute inflammation and clusters of mesothelial cells with reactive-looking atypia, being negative for malignant cells.
Carcinoembryonic antigen (CEA) was found to be elevated 21.53 ng/ml. In addition, serologies for human immunodeficiency virus, Mycoplasma pneumoniae, cytomegalovirus, Epstein Barr and Chlamydia pneumoniae were negative except for IgM to cytomegalovirus which was positive.
A chest CT scan showed two pathologically sized mediastinal adenopathies of pretracheal location measuring approximately 19 x 15 mm and 18 x 17 mm respectively, and a slightly larger bilateral pleural effusion on the right side. A pulmonary window showed bilateral and diffuse alterations of the lung parenchyma with an interstitial pattern of nodular septal reticulum and lobular centre with areas of patchy alveolar condensation predominantly distributed in the apical segment of the lower lobes and both upper lobes.
Bronchoscopy was performed, observing upper airways, vocal cords and trachea without alterations, there was a widening in the subcarinal area. The bronchial tree showed no alterations. Bronchoalveolar lavage was performed in the apical segment of the culmen, but the examination had to be suspended due to poor tolerance, and neither puncture of the adenopathies nor transbronchial biopsy could be performed.
The pathological anatomy of the lavage revealed abundant macrophages and epithelial groups with reactive atypia, compatible with type II pneumocyte hyperplasia, secondary to acute lung damage.
It was thought that he might have diffuse interstitial lung disease (DIDD) due to the anatomopathological, clinical and radiological features. The first possibility was eosinophilic pneumonia due to the presence of eosinophilia in peripheral blood, and treatment was started with prednisone 1 mg/kg body weight, with a favourable evolution, and he was discharged 25 days after admission, without fever or dyspnoea.
Seven days later, the patient presented again with a cough with mucous expectoration and later haemoptysis. Chest X-ray showed no changes, so a chest CT scan was performed, which revealed a ground glass pattern and a moderate bilateral pleural effusion.
It was decided to perform a lung biopsy to obtain the diagnosis. The report was diffuse lymphatic permeation (following a nodular interstitial pattern) by a well-differentiated acinar-papillary adenocarcinoma with abundant psammoma bodies. Cells with malignant cytological features compatible with adenocarcinoma were observed in the pleural fluid. Histochemical tests confirmed the pulmonary origin of the adenocarcinoma.
She is currently undergoing chemotherapy with the combination of cisplatin and gemcitabine.
Two cycles have been administered so far, so we do not yet have data on the possible response.
