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Case Report |
1
Department of Radiology, Stanford University Medical Center, Rm. S072A, 300
Pasteur Dr., Stanford, CA 94305-5105.
2
Department of Pathology, Stanford University Medical Center, Stanford, CA
94305-5105.
3
Division of Pulmonary and Critical Care, Stanford University Medical Center,
Stanford, CA 94305-5105.
Received February 6, 2001;
accepted after revision April 24, 2001.
Address correspondence to A. N. Leung.
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Five days after a peripherally inserted central catheter was placed for the daily prostaglandin infusions, the patient became febrile, with blood cultures positive for Klebsiella pneumoniae and Enterobacter cloacae. His temperature defervesced after initiation of the appropriate antibiotics and an exchange of the central line. Seven days after finishing the course of antibiotics, the patient again developed the same gram-negative bacteremia. On an abdominal CT scan ordered to exclude an intraabdominal source of sepsis, multiple 1- to 3-mm pulmonary nodules were identified in the visualized lung bases. A dedicated high-resolution CT scan of the thorax showed an enlarged main pulmonary artery measuring 3.0 cm in diameter and innumerable centrilobular nodules, some with a tree-in-bud appearance that were scattered diffusely in the lung parenchyma (Figs. 1A and 1B). The patient declined further workup of his lung disease and left the hospital with a course of IV antibiotics to be finished on an outpatient basis.
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Five days after hospital discharge, the patient re-presented to the emergency room febrile, hypotensive, and in respiratory failure, requiring emergency intubation. A chest radiograph obtained at admission showed a diffuse bilateral reticular pattern. Pulmonary artery catheterization revealed pulmonary artery hypertension with a blood pressure of 80 over 44 mm Hg, a decreased cardiac output of 2.7 L, and an elevated wedge pressure of 19 mm Hg. Clinically, the patient was believed to have pulmonary edema associated with decompensated pulmonary artery hypertension. After treatment with empiric antibiotics, vasodilators, and diuretics, the patient became stabilized, allowing extubation. A subsequent thoracoscopic biopsy of the right lower lung lobe showed innumerable sharply delineated nodules centered in or around the pulmonary arterioles and muscular pulmonary arteries and ranging from 0.1 to 0.4 mm in diameter (Fig. 1C). Many of the vessels showed alternating dilatation and disruption of elastic lamina and musculature with replacement by granulomatous nodules and fibrosis (Fig. 1D). The intravascular and perivascular foreign body granulomas contained refractile pale crystals measuring 20-95 µm that were optically active under polarizable light (Fig. 1E). The crystals stained violet on a predigested periodic acid—Schiff stain, black on Gomori methenamine-silver stain, and orange on Congo red stain. Admixed with the crystals were variable numbers of histiocytes and foreign body—type giant cells and occasional aggregates of deeply basophilic amorphous material resembling charred tissue. Histologic sections of a Vicodin tablet displayed identical crystalline material. On directed questioning, the patient admitted to IV injection of his prescribed oral medications.
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Clinical symptoms associated with cellulose granulomatosis are largely dependent on the extent of arteriolar involvement and the severity of the induced pulmonary artery hypertension; symptoms may range from none to exertional dyspnea to sudden death [4, 5]. On high-resolution CT, the findings of cellulose granulomatosis have been previously described as diffuse 1- to 2-mm interstitial nodules [6], some of which occur in a centrilobular distribution [7]. In our biopsy-proven case, nodules ranged from 1 to 3 mm, were centrilobular, and were associated with a tree-in-bud pattern.
The descriptor "tree-in-bud" was first applied to the appearance of micronodules distributed at the termination of bronchovascular bundles identified on high-resolution CT in patients with diffuse panbronchiolitis [8]. Since the initial description of tree-in-bud pattern, its differential diagnosis has remained largely limited to bronchiolar diseases in which the bifurcated or budding structures represent thick-walled or dilated bronchioles filled with mucus, fluid, or pus. Entities often included in the differential diagnosis are infectious bronchiolitis, respiratory bronchiolitis, constrictive bronchiolitis, and aspiration pneumonia. To our knowledge, our case is unique in that it is a pathologically proven case of a tree-in-bud appearance on CT caused by arteriolar disease. As documented by the histologic findings, the micronodules creating the bifurcating structures seen on high-resolution CT in patients with cellulose granulomatosis represent intraarteriolar accumulation of micro-crystalline cellulose with associated adjacent granulomatous reaction.
In summary, the CT manifestations of cellulose granulomatosis consist of diffuse centrilobular nodules and a tree-in-bud pattern. In the differential diagnosis of a tree-in-bud pattern, arteriolar diseases, such as cellulose granulomatosis, should be considered in addition to the more common small airways diseases, especially in the setting of pulmonary artery hypertension or IV drug abuse.
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