Last Updated

17 Nov 2002

    Source: Krol CM. Dynamic CT Features of Inhalational Anthrax Infection. American J Roentgenology 178(5), May, 2002.

A 61-year-old woman with a history of hypertension presented to the emergency department complaining of worsening shortness of breath, dyspnea at rest, and substernal pain that had begun 3 days earlier. Associated chills and cough productive of blood-tinged sputum were noted. Physical examination revealed an alert and oriented woman with a respiratory rate of 38 breaths per minute and a temperature of 36.0°C. Diffuse bilateral rales were noted at chest auscultation. Blood tests revealed a WBC of 11.4 x 10⁹/L (normal range, 4.5-11.0 x 10⁹/L), lactate dehydrogenase of 1370 U/L (normal range, 50-200 U/L), aspartate aminotransferase of 240 U/L (normal range, 20-48 U/L), alanine aminotransferase of 263 U/L (normal range, 10-40 U/L), and a normal coagulation profile.

Fig. 1A. 61-year-old woman with history of hypertension who presented to emergency department with worsening shortness of breath, dyspnea at rest, and substernal pain that had begun 3 days earlier. Initial anteroposterior upright chest radiograph shows widened superior mediastinum, bilateral perihilar infiltrates, and pleural effusions.

A portable anteroposterior upright radiograph of the chest obtained shortly after presentation revealed marked widening of the superior mediastinum. Bilateral perihilar opacities were present, and moderate pleural effusions with fluid in the minor fissure (see Figure 1A) were detected. Therapy for congestive heart failure was initiated; however, several hours later, a bedside echocardiogram showed a normal ejection fraction and wall motion with mild pericardial effusion. The patient was then given levofloxacin for atypical pneumonia.

While in the emergency department, the patient developed respiratory failure requiring mechanical ventilation, placement of a pulmonary artery catheter, and transfer to the intensive care unit.

Fig. 1B. Supine chest radiograph obtained 12 hr after Fig 1A shows further widening of mediastinum, marked hilar enlargement, and apparent increase in pleural effusions.

A second portable anteroposterior supine chest radiograph obtained approximately 12 hr after presentation revealed further widening of the mediastinum. Marked hilar enlargement was visible. An exact size comparison of the pleural effusions on this chest radiograph with those on the earlier chest radiograph was difficult because the patient's position had changed, but the effusions appeared to have increased in size (see Figure 1A). Blood samples were collected for Gram staining and cultures.

Contrast-enhanced CT was performed approximately 16 hr after presentation to evaluate for possible anthrax infection and to rule out pulmonary embolism (see Figures 1C, 1D, 1E, and 1F).

Fig. 1C. Dynamic CT scan obtained 16 hr after Fig 1A at level of left atrium shows large bilateral pleural effusions with high-density material (white arrows) on dependent right pleural surface. Note amount of heterogeneous material in mediastinum, compressing the hilar vessels and left atrium (black arrows).

Fig. 1D.  Initial axial CT scan obtained at level of aortic arch shows extensive paratracheal tissue and edema (arrows) infiltrating mediastinal fat.

Fig. 1E. Magnified CT scan obtained at subcarinal level shows bronchial mucosal thickening (arrows).

Fig. 1F. CT scan obtained using lung window settings on exhalation shows perihilar opacities with sparing of peripheral lung segments.

The CT scanner (CTi; General Electric Medical Systems, Milwaukee, WI) was set at 140 kVp and 260 mA/sec with a 3-mm collimation and a pitch of 2.0, and CT was performed after the IV administration of 150 mL of IV contrast material (Omnipaque [iohexol] 300 mg I/mL; Nycomed, Princeton, NJ), which was injected at a rate of 3.5 mL/sec after a 25-sec delay. Additional CT images of the entire chest were obtained with a collimation of 7 mm (see Figures 1G and 1H) 20 min after the initial injection of contrast material.

Fig. 1G. CT scan obtained 20 min after initial contrast bolus through subcarinal region shows confluent, ill-defined ringlike areas of enhancement (arrows). Note central hypodensity associated with hemorrhagic lymphadenopathy.

The initial CT scan revealed large bilateral pleural effusions measuring 13 H. A small amount of high-density material, measuring 37 H, was visible in the dependent aspect of the right pleural space. A large amount of heterogeneous material was present in the mediastinum from the thoracic inlet to the level of the diaphragm. The material had density measurements ranging from 18 to 64 H. Most of the lung was collapsed because of compression exerted by the large pleural effusions. No mediastinal fat planes were visualized, and compression of the left atrium and the hilar vessels (see Figure 1C) was evident. Moreover, encasement of the trachea and esophagus by soft tissue and edema (see Figure 1 D) was noted. Mucosal thickening was seen in the bronchial airways (see Figure 1E). Images obtained using lung window settings revealed peribronchial opacities. The periphery of the aerated portion of the lungs was free of visible infiltrate. Bilateral hilar adenopathy was also present (see Figure 1F). A 4.2-cm, smooth-walled aneurysm of the ascending aorta (see Figures 1D and 1F) was identified; this finding was thought to be incidental. No pulmonary embolism was present.

On the delayed CT images, ill-defined ringlike areas of enhancement of variable size with central hypodensity were clearly visible throughout the mediastinum and hilar regions (see Figure 1G).

Fig. 1H. Delayed CT scan shows pericardial effusion (open arrows) and paraesophageal hemorrhagic adenopathy (solid arrows).

Marked paraesophageal adenopathy and moderate pericardial fluid with a density of 43 H, which was unchanged from the initial CT scan (see Figure 1H), were visible. Comparative density measurements of the same locations using images obtained at the same levels showed increases of approximately 20 H. The mediastinal findings were considered to represent hemorrhagic lymphadenopathy and edema. The diagnosis of inhalational anthrax was suspected given the rapid clinical progression and the presence of mediastinal edema and hemorrhage on CT in the absence of a recent traumatic event. The patient was started on additional antimicrobial coverage to include rifampin and clindamycin. Chest tubes were placed; the tubes drained serosanguineous fluid from the pleural space—approximately 2.0 L from the right and 1.0 L from the left. The pleural fluid was composed of 7.3 x 109/L RBC, 3 x 109/L WBC, 42 g/L protein, 1264 U/L lactate dehydrogenase, and 8.2 mmol/L glucose. Bronchoscopy performed several hours after CT showed diffusely hemorrhagic and friable tracheal and bronchial mucosa. Gram-positive rods were found at Gram staining. Cultures of blood and pleural fluid grew B. anthracis that was confirmed by polymerase chain reaction. Despite aggressive antimicrobial and supportive therapy, the patient experienced multiorgan failure with disseminated intravascular coagulopathy. She developed cardiac tamponade, became hemodynamically unstable, and died despite resuscitative efforts on the fourth hospital day. (The detailed clinical assessment and treatment of the patient in this case was recently reported in the Journal of the American Medical Association)

Autopsy revealed marked mediastinal, perihilar, and peribronchial lymphadenopathy. The nodes were darkly pigmented with a hemorrhagic coating of the capsule, and extensive hemorrhage and thrombus were within the nodes. Diffuse tracheobronchial mucosal edema, hemorrhage, and large amounts of bloody pleural and pericardial fluid collections were found. Pulmonary edema was present with no focal infiltrates (Gill JR, personal communication).

Return to Case 22