**2. Clinical presentation**

Bacterial pneumonia and pulmonary infarction frequently mimic each other clinically, indicates that most methods for distinguishing between these illnesses are unsatisfactory. Both diseases may give rise to dyspnea, pleuritic pain, tachypnoea, fever, cyanosis, hypotension, cough, hemopthysis, jaundice, leukocytosis and similar radiographic abnormalities (8).

Shaking chills point strongly to bacterial pneumonia. Additional hints are a preceding upper respiratory tract infection followed by gradually increasing malaise and then cough, usually

Cavitary Pulmonary Infarct: The Differential Diagnostic Dilemma – A Case Report 217

reveals right ventricular dilatation, septal deviation of left ventricle, tricuspidal

Pulmonary function test and arterial blood gas studies provide data that are too variable

Radiographic similarities of bacterial pneumonia and pulmonary infarction are the chief source of diagnostic confusion between the two entities. Each is responsible for parenchymal infiltrates of varied size and shape, with or without pleural effusion, atelectasis or cavitation. In contrast to bacterial pneumonia, pulmonary infarcts always abut a pleural surface and predominate in lower lobes, especially the right. They also may appear in concert with dilatation of one or both main pulmonary arteries, decreased peripheral vascular markins in the affected portion of lung (oligemia) or engorged vassels in the non affected areas (pleonemia). Further radiographic clues to pulmonary infarction are infiltrates appearing first in one lung and then the other or "pneumonia" unresponsive to

Spiral computed tomography and magnetic resonance angiography are helpful in establishing the difference between pneumonia and pulmonary infarct. Also, this imaging techniques could help tracking the resolution of the thrombo emboli, but they are expensive

Pulmonary arteriography is the most specific means of differentiating bacterial 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

The grater the size of infarct, more likely its centre will be hypoxic and nectrotic. Pulmonary

The median time from the first detection of consolidation to cavity formation is 14 days (12). Doppler sonography is a noninvasive and convenient tool for diagnosing pulmonary embolism and follow-up reperfusion of the lung. Dynamic changes in blood flow in

Despite use of the aforementioned techniques, the question of infected versus infracted lung sometimes will persist. To minimize error, the physicians should think of both diseases when he considers either, particularly if the process involves the lower lobes, especially the right. Dangers of delaying treatment for pulmonary infarction rival the hazards of withholding specific chemotherapy in bacterial pneumonia. Thus, as long as the diagnosis

Multiple complications have been associated with pulmonary infarct, including pneumonia, empyema, pneumothorax, lung abscess, bronchopleural fistulae and lethal haemorrhage.

The mortality rate is as high as 41% and 73% for nonifected and infected cavitary pulmonary infarcts, respectively. Anticoagulants and antibiotics are the mainstay of therapy. Massive haemopthysis may persist even after discontinuation of anticoagulants. Possible explanation for this phenomenon are an overdose of anticoagulants and reperfusion of necrotic lung tissue. Anticoagulants use in cavitary pulmonary infarction, therefore, must be very carefully monitored and causation should be exercised in monitoring clinical conditions and

and nonspecific to differentiate bacterial pneumonia from pulmonary infarction (8).

regurgitation or right ventricle hypokinesis with wall thinning (8, 11).

infarction they contain filling defect, appear obstructed, or both (8).

infarct larger than 4 x 4 cm in size have a great tendency for cavitation (12).

consolidated areas provides information about the status of reperfusion (6).

remains in doubt, treatment for both disorders seems well advised (8).

Large series of autopsies reveald cavitation in 4-5% of all pulmonary infarcts (5).

**4. Imaging studies** 

chemotherapy (8).

and unavailable in many hospitals (6,7).

the status of coagulation (10).

productive of purulent sputum. Patients with pulmonary infarction more often become ill with dramatic suddenness, seldom have a cough and experience shaking chills only if the emboli are septic or the infarct become infected (8).

Physical signs are not specific for either diseases. Although high fever is more typical of bacterial pneumonia, it is occurs with sufficient frequency in pulmonary infarction to be unreliable as differential diagnostic sign. Patients with pulmonary infarction, as compared to those with bacterial pneumonia, generally are more dyspnoic and tachypnoic in relation to the extent of their physical and radiographic abnormalities and rarely exhibit classic signs of consolidation. They more often manifest hypotension, either transient or recurrent, and more commonly show signs suggesting pulmonary hypertension and right-sided congestive heart failure, e.g. a loud pulmonis component of the second heart sound and elevation of the jugular venous pressure (8).

A pleural friction rub helps in differentiation only when chest radiography shows no parenchymal disease. Then, infarction is more often do not cause radiographic changes early in the course of the illness (8).
