**4. Imaging studies**

216 Venous Thrombosis – Principles and Practice

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

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

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

Sputum examination is one of the best ways of differentiating bacterial pneumonia from pulmonary infarction. In bacterial pneumonia the sputum classically is purulent, occasionally foul smelling and may contain bright red fleck of blood. Gram's stain typically shows many bacteria and polymorphonuclear leukocytes. In pulmonary infarction, sputum, when present, usually is frankly blood with few bacteria or inflammatory cells. If the infarct becomes infected the sputum may be indistinguishable from that in bacterial pneumonia. Blood cultures often reveal the causative microorganism in the patients with bacterial

Cavitation after bland pulmonary infarcts may result from either aseptic necrosis of the infracted lung or from secondary bacterial infection with subsequent abscess formation. It is

Two types of infected pulmonary infarct have been proposed based on the mode by which infection sets in (10). One is called "primary" because the infection is from a septic embolus. The other is called "secondary" because the infection is bronchigenic origin. Some authors suggest that the development of fever and/or purulent sputum following a pulmonary infarct is highly suspicious for secondary infection. The spectrum of causative agents for

Total leukocyte count has limited discriminatory value. It usually is normal or slightly elevated in pulmonary infarction, but there is reports of leukocytes count higher than 40 000 per mm3 in patients with massive, bland necrosis of pulmonary tissue. Elevated serum lactic dehydrogenase (LDH) activity, normal aspartate aminotranspherase activity (AST) and increased serum bilirubin concentration forms a triad once considered a sensitive indicators of pulmonary embolism and infarction. However, subsequent studies have shown that these tests fail to differentiate pulmonary infarction from pneumonia and host of

Electrocardiographic abnormalities that may appear are right ventricular conduction disturbances; right axis deviation; inverted T-waves with S-T segment deviation in the right precordial leads; peaked T-waves in leads II, III and AVF; various types of supraventricular and raraly ventricular arrhythmias and S1, Q3 or S1,S2, S3 patterns. Heart ultrasound may

pneumonia but show no growth in cases of bland pulmonary infarction (8).

infected pulmonary infarct is similar to that of nosocomial pneumonia (3).

emboli are septic or the infarct become infected (8).

**3. Laboratory and other diagnostic tests** 

infective almost as often as it is aseptic (9).

other disorders (8).

jugular venous pressure (8).

in the course of the illness (8).

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 chemotherapy (8).

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 and unavailable in many hospitals (6,7).

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

The grater the size of infarct, more likely its centre will be hypoxic and nectrotic. Pulmonary infarct larger than 4 x 4 cm in size have a great tendency for cavitation (12).

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

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

Multiple complications have been associated with pulmonary infarct, including pneumonia, empyema, pneumothorax, lung abscess, bronchopleural fistulae and lethal haemorrhage. Large series of autopsies reveald cavitation in 4-5% of all pulmonary infarcts (5).

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 the status of coagulation (10).

Cavitary Pulmonary Infarct: The Differential Diagnostic Dilemma – A Case Report 219

Fig. 1. Initial chest PA (postero-anterior) radiography showing enlarged cardiac shadow

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

without pulmonary opacities
