**5. Case presentation**

Patient was admitted to our clinic with a three week history of dyspnea, tachycardia, cough, expectoration of yellow colored sputum, fever, exhaustion and lower legs edema. Few days before admission to clinic he presented altered level of consciousness (mental confusion), caused by alcohol withdrawal. The patient suffered from congestive heart failure and chronic obstructive pulmonary disease for several years. There was no past medical history of predisposition factors for embolism or episodes of venous thrombo-embolism.

On examination he presented normal mental status, body temperature was within normal range, blood pressure 130/80 mmHg, pulse rate 90 beats/min; respiratory rate 26 breath/min; with signs of peripheral cyanosis. The chest expanded symmetrically and breathing sounds were clear. There were heart rhythm disorder (absolute arrhythmia) but no heart murmurs were detected. The liver and spleen were not palpable. Lower leg edema was noticed.

The initial laboratory blood test revealed elevated inflammatory parameters: white blood cells:15.7 x 109/L; with 87.6% neutrophils; 3.4% monocytes and 9.0% lymphocytes; Creactive protein: 73 mg/L; D-dimer: 759 ηg/ml. The prothrombin time, activated partial thromboplastin time (PTT) and platelets were within normal range. There were elevated activity of aspartate aminotranspherase (160.6 U/L); alanin aminotransferase (128.0 U/L); lactic dehydrogenase (745 U/L); serum bilirubin concentration (45 μmol/L);blood urea nitrogen (16.3 mmol/L) and creatinine (120.4 μmol/L). But, all this test has limited discriminatory value.

The arterial gas blood analysis showed the following: pH 7,5; carbon dioxide tension in arterial blood (PCO2) 31 mmHg; oxygen tension in arterial blood (PO2) 71 mmHg; HCO3 24 mmol/L; BE 1 mmol/L and oxygen saturation (SaO2) 95%.

Lung functional test shown severe restrictive ventilation disorder (FEV1: 8%; FVC: 44% - 1.67 L; FEV1/FVC: 72%) which is nonspecific to differentiate bacterial pneumonia from pulmonary infarction as well as the arterial gas blood analysis too.

The electrocardiography (ECG) revealed atrial fibrillation only. The initial chest radiograph was showed enlarged cardiac shadow without pulmonary opacities (**Figure 1**) because infarction is more often do not cause radiographic changes early in the course of the illness. Congestive heart failure was diagnosed and the patient was treated with diuretics and inotropes.

However, a ten days later the intensity of dyspnea, fatique, weakness and exhaustion has increased. He was febrile (38.30 C). A contribution to literature data, in our case, clinical condition has got worsening suddenly. Chest radiography was significant since it showed round pulmonary consolidation with central cavitation on the apical segment of the right lower lobe (**Figure 2**). The patient was placed on antibiotic therapy (intravenous ceftazidine and ertapenem) for a presumptive diagnosis of bacterial pneumonia.

However, one week later, the treatment with antibiotics was not satisfactory and there were no clinical recovery. Also, there were no microbiologic confirmation of causative microorganism which made definitive diagnosis difficult. The clinical symptoms of congestive heart failure was dominant and the patient underwent a cardiac ultrasound which revealed tricuspidal regurgitation and elevated right ventricular pressure (systolic blood pressure of right ventricule - SPRV: 46 mmHg). The increased intensity of dyspnoea, fatique, weakness and exhaustion, despite the treatment with diuretics and inotropes was due to unconfirmed hemodynamic disorder.

Patient was admitted to our clinic with a three week history of dyspnea, tachycardia, cough, expectoration of yellow colored sputum, fever, exhaustion and lower legs edema. Few days before admission to clinic he presented altered level of consciousness (mental confusion), caused by alcohol withdrawal. The patient suffered from congestive heart failure and chronic obstructive pulmonary disease for several years. There was no past medical history

On examination he presented normal mental status, body temperature was within normal range, blood pressure 130/80 mmHg, pulse rate 90 beats/min; respiratory rate 26 breath/min; with signs of peripheral cyanosis. The chest expanded symmetrically and breathing sounds were clear. There were heart rhythm disorder (absolute arrhythmia) but no heart murmurs were detected. The liver and spleen were not palpable. Lower leg edema

The initial laboratory blood test revealed elevated inflammatory parameters: white blood cells:15.7 x 109/L; with 87.6% neutrophils; 3.4% monocytes and 9.0% lymphocytes; Creactive protein: 73 mg/L; D-dimer: 759 ηg/ml. The prothrombin time, activated partial thromboplastin time (PTT) and platelets were within normal range. There were elevated activity of aspartate aminotranspherase (160.6 U/L); alanin aminotransferase (128.0 U/L); lactic dehydrogenase (745 U/L); serum bilirubin concentration (45 μmol/L);blood urea nitrogen (16.3 mmol/L) and creatinine (120.4 μmol/L). But, all this test has limited

The arterial gas blood analysis showed the following: pH 7,5; carbon dioxide tension in arterial blood (PCO2) 31 mmHg; oxygen tension in arterial blood (PO2) 71 mmHg; HCO3 24

Lung functional test shown severe restrictive ventilation disorder (FEV1: 8%; FVC: 44% - 1.67 L; FEV1/FVC: 72%) which is nonspecific to differentiate bacterial pneumonia from

The electrocardiography (ECG) revealed atrial fibrillation only. The initial chest radiograph was showed enlarged cardiac shadow without pulmonary opacities (**Figure 1**) because infarction is more often do not cause radiographic changes early in the course of the illness. Congestive heart failure was diagnosed and the patient was treated with diuretics and

However, a ten days later the intensity of dyspnea, fatique, weakness and exhaustion has increased. He was febrile (38.30 C). A contribution to literature data, in our case, clinical condition has got worsening suddenly. Chest radiography was significant since it showed round pulmonary consolidation with central cavitation on the apical segment of the right lower lobe (**Figure 2**). The patient was placed on antibiotic therapy (intravenous ceftazidine

However, one week later, the treatment with antibiotics was not satisfactory and there were no clinical recovery. Also, there were no microbiologic confirmation of causative microorganism which made definitive diagnosis difficult. The clinical symptoms of congestive heart failure was dominant and the patient underwent a cardiac ultrasound which revealed tricuspidal regurgitation and elevated right ventricular pressure (systolic blood pressure of right ventricule - SPRV: 46 mmHg). The increased intensity of dyspnoea, fatique, weakness and exhaustion, despite the treatment with diuretics and inotropes was

mmol/L; BE 1 mmol/L and oxygen saturation (SaO2) 95%.

pulmonary infarction as well as the arterial gas blood analysis too.

and ertapenem) for a presumptive diagnosis of bacterial pneumonia.

due to unconfirmed hemodynamic disorder.

of predisposition factors for embolism or episodes of venous thrombo-embolism.

**5. Case presentation** 

was noticed.

discriminatory value.

inotropes.

Fig. 1. Initial chest PA (postero-anterior) radiography showing enlarged cardiac shadow without pulmonary opacities

Fig. 2. PA (postero-anterior) chest radiography ten days from admission showing round pulmonary consolidation with central cavitation on the apical segment of the right lower lobe

Cavitary Pulmonary Infarct: The Differential Diagnostic Dilemma – A Case Report 221

The follow-up chest radiograph (three weeks later) showed regression of mentioned pulmonary opacities (**Figure 4**). Due to anticoagulant therapy was administered immediately after the findings of the CT scans were obtained, the patient was clinicaly

Fig. 4. Follow-up chest radiograph (three weeks later) showing regression of mentioned

Cavitary pulmonary infarct is a rare but frequently misdiagnosed disease entity. Differentation between cavitary pulmonary infarct and multiple complications or other diseases can be a real challenge because of the similar radiographic abnormalities and clinical presentation of all this conditions. In the cases with clinical suspicion to "pneumonia" unresponsive to chemotherapy images studies are of great help. The best evidence of infarction is the angiographic demonstration of pulmonary thromboemboli. Anticoagulant and antibiotic treatment in the cases of infected cavitary pulmonary infarct

The authors wish to thanks all physicians from the clinic who participated in the medical care of the patient described in this report. Also, we are grateful to Marta Djordjevic for

must be started immediately after the diagnosis is established.

technical assistance in the computer processing of the images.

pulmonary opacities.

**7. Acknowledgement** 

**6. Conclusion** 

recovered and he was discharged with follow-up recommended.

The most striking and unexpected findings was contrast-enhanced computed tomography (CT) scan of blood vessels and identification of filling defect in the main pulmonary arteries which presumptive diagnosis of pneumonia excluded. There were pulmonary consolidation with central cavitation on the right lower and left upper lobes too. The diameter of right and left consolidation was 63 x 75 mm and 85 x 70 mm respectively (**Figure 3a and 3b**). The size of pulmonary infarct , in our case, is grater than 40 x 40 mm which explain the appearance of cavitation. Also, the velocity of cavity formation presented in our case is significantly lower than literature data pointed out. Venous duplex ultrasound of lower extremitas was negative for deep-vein thrombosis. Low-molecular heparin were administered immediately after the findings of the CT scans were obtained.

Fig. 3a. and 3b. Contrast - enhanced computed tomography scan of blood vessels showing filling defect in the main pulmonary arteries with central cavitation on the right lower and left upper lobes too

The follow-up chest radiograph (three weeks later) showed regression of mentioned pulmonary opacities (**Figure 4**). Due to anticoagulant therapy was administered immediately after the findings of the CT scans were obtained, the patient was clinicaly recovered and he was discharged with follow-up recommended.

Fig. 4. Follow-up chest radiograph (three weeks later) showing regression of mentioned pulmonary opacities.
