SESSION TYPE: Miscellaneous Global Case Report Posters
PRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION: Pulmonary infarction is localized necrosis of lung tissue by obstruction of the arterial blood supply. In the case of infection as developing complication, pulmonary infarction can mimic necrotizing pneumonia clinically.
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. The patient suffered from congestive heart failure and 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 clinical signs of congestive heart failure and heart rhythm disorder. The initial laboratory blood test revealed elevated inflammatory parameters; parameters of coagulation status were within normal range and there were elevated hepatic and renal function parameters. The arterial gas blood analysis was within normal range and lung functional test shown severe restrictive ventilation disorder. The initial chest radiograph was showed enlarged cardiac shadow without pulmonary opacities and congestive heart failure was diagnosed. Due to clinical deterioration and presence of round pulmonary consolidation with central cavitation on the apical segment of the right lower lobe on chest radiography, patient was placed on antibiotic therapy for a presumptive diagnosis of necrotizing pneumonia. However, there were no clinical recovery. The clinical symptoms of congestive heart failure was dominant and cardiac ultrasound which revealed tricuspidal regurgitation and elevated right ventricular pressure. 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. 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. The follow-up chest radiograph (three weeks later) showed regression of mentioned pulmonary opacities, the patient was clinicaly recovered and he was discharged with follow-up recommended.
DISCUSSION: Necrotizing pneumonia and pulmonary infarction frequently mimic each other clinically. The increased intensity of dyspnoea, fatique, weakness and exhaustion, observed in our patient, despite the treatment with diuretics and inotropes was due to unconfirmed hemodynamic disorder. Laboratory blood tests, pulmonary function tests and arterial blood gas studies provide data that are too variable and nonspecific for differential diagnosis. The chief source of diagnostic confusion between the two entities are radiographic similarities. Each is responsible for parenchymal infiltrates of varied size and shape, with or without pleural effusion, atelectasis or cavitation. Infarction is more often do not cause radiographic changes early in the course of the illness, found in our case too. Contrast-enhanced computed tomograpgy (CT) scan of blood vassels is the most specific means of differentiating necrotizing pneumonia from pulmonary infarction. In bacterial pneumonia the pulmonary arteries proximal to the subsegmental level show neither filling defect nor obstructive lesions, where in pulmonary infarction they contain filling defect, appear obstructed, or both as in our case. Clinical recovery and chest radiograph regression of pulmonary opacites is due to anticoagulant therapy was administered immediately after the findings of the CT scans were obtained.
CONCLUSIONS: Differentation between cavitary pulmonary infarct and necrotizing pneumonia as complication can be a real challenge because of the similar radiographic abnormalities and clinical presentation of bouth conditions. The best evidence of infarction is the angiographic demonstration of pulmonary thromboemboli. Anticoagulant and antibiotic treatment in the cases of infected cavitary pulmonary infarct must be started immediately after the diagnosis is established.
1) Robert Baird, Pulmonary Embolism and Infarction; January 19, 2008 (www.americanchronicle.com)
2) Djordjevic I et all. Difficulties in establishing a timely diagnosis of pulmonary artery sarcoma misdiagnosed as chronic thrombo-emblic pulmonary disease: a case report. JMCR 2009; 3:64.
3) Lennox H Huang, MD, Pulmonary Infarction; Aug 12, 2008 (www.emedicine.com)
DISCLOSURE: The following authors have nothing to disclose: Ivanka Djordjevic, Tatjana Pejcic, Desa Nastasijevic-Borovac, Tatjana Radjenovic-Petkovic
No Product/Research Disclosure InformationClinical Center-Nis, Clinic for Lung Diseases, Nis, Serbia