Case Report

A 83-year-old man was admitted to the hospital with a 16 weeks history of progressively increasing breathlessness, and leg swelling which inhabitited him to walk. There was no history of cough, sputum or chest pain. He had a medical history of polymyalgia rheumatica 6 years before admission, high blood pressure and non-insulin-dependent diabetes mellitus. He had received prednisone 30 mg/d, digoxin 0,50 mg/d five times a week, enalapril 20 mg/d and furosemide 40 mg/day. On physical examination, he was tachyneic with a respiratory rate 26 breats per minute. His temperature was 38°C; blood presure was 120/50 mm Hg and the pulse rate was 100 beats per minute. The jugular venous pressure was normal. The heart examination revealed systolic blow.

The lung examination revealed crepitations in over the right lower zone. Examination finding of other systems and neurologic test were normal. Blood test gave the following results: white blood cell count 10900/µL (68 neutrophils), the hemoglobin level was 9 g/dL, hematocrit 28%; VCM 85 fl and the platelet count was 164 x 10 ³ /µL. An erythrocyte sedimentation rate was of 121 mm/h; C-reactive protein were 6,7 mg/dl (normal range 0,0-0,5). Glucose 121 mg/dL; creatinine 1,7 mg/dL. Serological markers for HIV virus and blood culture were negatives. Other laboratory investigations performed at his admission at hospital included electrolytes and liver function tests, coagulation studies and serum protein electrophoresis were within all normal limits.

Results of arterial blood gas analysis on room air showed the following: ph 7,43; Pa CO₂ 46; Pa O₂ 65; HCO₃Na 30; Saturation 93% Electrocardiogram shown sinus rhythm a 100 beats per minute and left bundle branch block. Transthoracic echocardiography showed only left ventricle hipertrophic with adequate left ventricular ejection fraction. His chest radiograph showed cavitary lung lesion in the medium lobe (Figure 1). Subsequent computed tomography of the chest revealed a 4,5 cm cavitary lesion in the middle lobe which had developed progressively in pleura, bronchial and vessels. No associated mediastinical adenopathy was evident (Figure 2) . An empirical treatment with intravenous cefotaxime 2 g every 6 hours, intravenous clindamycin 500 mg three times a day and subcutaneous low-molecular-weitgh heparin at a dose of 1mg/k/12 hours was started.

Figure 1

Figure 1: Chest roentgenogram of 84 year-old man demostrating cavitary pulmonary lesion in the medium lobe.

Figure 2

Figure 2: Computed tomography, showing a 4,5 cm cavitary lesion in the middle lobe, which affects to pleura, bronchial and vessels.

A bronchoscopy and a Doppler echocardiography of his legs were done . The bronchoscopy did not show any endobronchial lesion and test of bronchoalveolar lavage fluid for citology, bacteria, mycobacteria, were negatives. Doppler echocardiography showed deep vein thrombosis in both iliac, femoral, and popliteal veins. On finished the antibiotic treatment and the oral anticoagulants were started. At follow-up 6 months later, the patient was asyntomatic and the cavitary pulmonary lesion and the deep vein thrombosis had disappeared.

Discussion

Cavitary lung disease results from various causes (₁,₂,₃,₉). In our immunocompromised patient, infectious causes were certainly considered: mycobacterial, fungal, gram-negatives necrotizing infection, anaerobic organisms were sought. Noninfectious causes such primary or metastatic neoplasms, pulmonary sequestration, granulomatous vasculitis must also be considered. However, in immunocompromised hosts, they would be of lower probability (₉). Cavitary pulmonary infarction is rare, which produce significant morbilidity and mortality (₁,₂,₅,₈,₁₀).

The infarction is uncommon because the lung has two blood supplies, through the bronchial and pulmonary arteries (₆). Our case, the computed tomography of the chest reveled invasion of the bronchial and pulmonary vessels for the lung cavitary lesion. After infarction occurs, cavitation can follow as a result of either aseptic liquefaction or secundary infection, which occurs by direct infection with bronchial organisms, aspiration of orally administered fluid, or hematogenous spread (₅,₉). Clinical symptoms and signs of cavitary infarct are nonspecific. Cavitary infarcts have been resected as suspected bronchogenic carcinoma, tuberculosis, complicated bacterial infection and anaerobic abscess (₆,₉,₁₀). However, pulmonary infarction is other likely cause, overcoat in immunocomprosed hosts (₆,₈,₉). The appearance of a cavity in an infarcted lung, especially when a fluid level is present, raises the suspition of abscess formation. However, the absence of symptoms of infection, as well as the negative sputum culture made de diagnosis of a septic process unlikely (₉).

We think that aseptic necrosis with cavitary formation may not be as rare as been believed hittherto; it should be considered in the differential diagnosis of pulmonary cavitation.

Correspondence to

Araceli Jimeno Sainz. C/ Luis Guedea n° 19, 3A. 50300 Calatayud (Zaragoza). Spain Tfno +34-660298525 E-mail: ajimenos@salud.aragon.es