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Case Report |
1 Department of Diagnostic Radiology, Lenox Hill Hospital, 100 E. 77th St., New
York, NY 10021.
2 Department of Internal Medicine, Division of Critical Care Medicine, Lenox
Hill Hospital, New York, NY 10021.
Received November 14, 2001;
accepted after revision February 26, 2002.
Address correspondence to C. M. Krol.
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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. 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 (Fig. 1B). Blood samples were collected for Gram staining and cultures.
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Contrast-enhanced CT was performed approximately 16 hr after presentation to evaluate for possible anthrax infection and to rule out pulmonary embolism (Figs. 1C,1D,1E,1F). 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 (Figs. 1G and 1H) 20 min after the initial injection of contrast material. 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 (Fig. 1C) was evident. Moreover, encasement of the trachea and esophagus by soft tissue and edema (Fig. 1D) was noted. Mucosal thickening was seen in the bronchial airways (Fig. 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 (Fig. 1F). A 4.2-cm, smooth-walled aneurysm of the ascending aorta (Figs. 1D and 1E) was identified; this finding was thought to be incidental. No pulmonary embolism was present.
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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 (Fig. 1G). Marked paraesophageal adenopathy and moderate pericardial fluid with a density of 43 H, which was unchanged from the initial CT scan (Fig. 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 [4].)
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).
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The largest epidemic of inhalational anthrax infection occurred in 1979 in Sverdlovsk, Russia, after the accidental release of aerosols of B. anthracis at a secret biologic-agent production facility. Forty-two autopsies, representing most of the fatalities, consistently revealed hemorrhagic necrosis of thoracic lymph nodes and hemorrhagic mediastinitis and other signs of increased vascular permeability including gelatinous edema of the mediastinum, pleural effusions, and pulmonary edema [10, 11].
In the United States, humans in the past have acquired inhalational anthrax by agricultural or industrial exposure. Only 18 cases of inhalational anthrax were reported in the United States from 1900 to 1978, making a single case a cause for alarm today [8]. Since October 3, 2001, the Centers for Disease Control and Prevention (CDC) has been investigating cases of bioterrorism-related anthrax infection. At the time of this writing, the CDC had identified 10 patients with suspected inhalational anthrax associated with an intentional release. In a CDC analysis of the patients with confirmed or suspected inhalation anthrax infection, all had abnormal findings on chest radiographs. Of the eight patients who underwent CT, all had mediastinal widening, lymphadenopathy, and paratracheal and hilar fullness. Pleural effusions were the only abnormality on the chest radiographs of the two patients who did not undergo CT. The pleural effusions were large and hemorrhagic, requiring frequent drainage. Radiographs typically showed mediastinal widening, prominent lung markings with peribronchial infiltrates, and pleural effusions [3].
The differential diagnosis of mediastinal widening with large pleural and mediastinal fluid collections in the acutely ill patient typically includes iatrogenic or noniatrogenic trauma, rupture of aortic aneurysm, or esophageal perforation. The cause of the findings in this patient was not clear on the initial CT scan, and additional images were therefore obtained 20 min later. The delayed CT scan effectively delineated innumerable confluent mediastinal and hilar lymph nodes with enhancing rims and hypodense centers, typical of necrosis or, as in this patient, hemorrhage and edema. The measured density of many of the mediastinal nodes increased between the initial and delayed CT scans. The cause of delayed nodal enhancement is not clear; however, altered lymph node hemodynamics due to rapid nodal enlargement and vascular compromise may play a role in the flow of contrast material into and out of the lymph nodes. Although the differential diagnosis for adenopathy and pleural effusions can include numerous entities—lymphoma, metastases, tuberculosis, or rare entities such as Castle-man's disease, the presence of mediastinal widening, diffuse ring-enhancing adenopathy, and pleural and mediastinal fluid collections may indicate inhalational anthrax infection, particularly in a patient with rapid clinical deterioration. Immediate serum diagnostic tests for diagnosing anthrax such as enzyme-linked immunosorbent assay and polymerase chain reaction are available only at national reference laboratories. Blood cultures may show growth in 6-24 hr [8]. CT therefore plays an important role in the rapid detection of mediastinal abnormalities associated with inhalational anthrax infection. Current CDC recommendations include chest CT for clinically suspect cases in the event that chest radiographs reveal normal findings [3].
In summary, advanced inhalational anthrax has unique clinical and radiographic features and presents on dynamic CT with diffuse hemorrhagic mediastinal and hilar adenopathy, mediastinal edema, bronchial mucosal thickening, perihilar infiltrates, and hemorrhagic pericardial and pleural effusions. If the case is severe enough, compression of the heart and perihilar vessels may be seen, as in this patient. Because patients present with nonspecific symptoms such as shortness of breath, chest pain, and cough, dynamic CT to rule out pulmonary embolism may be part of the initial workup. A delayed CT scan may delineate the hemorrhagic mediastinal lymph nodes, thus ensuring the diagnosis. Although only serologic examinations can confirm infection, these tests are too time-dependent in an illness with such rapid progression. Given the unpredictability of and the potential for future intentional exposure of the public to anthrax spores, familiarity with the CT findings of inhalational anthrax may allow earlier diagnosis and treatment.
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