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Bilateral Hilar Lymphadenopathy: An Uncommon Manifestation of Adult Tuberculosis

1977; Elsevier BV; Volume: 71; Issue: 3 Linguagem: Inglês

10.1378/chest.71.3.421

1931-3543

Arthur J. Sakowitz, Barry H. Sakowitz,

Mycobacterium research and diagnosis

Two patients with abnormal findings on roentgenograms, which included bilateral hilar lymphadenopathy, are presented. After extensive workup, they were found to have tuberculous infections. This uncommon roentgenographic presentation of adult tuberculous infection is discussed. Two patients with abnormal findings on roentgenograms, which included bilateral hilar lymphadenopathy, are presented. After extensive workup, they were found to have tuberculous infections. This uncommon roentgenographic presentation of adult tuberculous infection is discussed. Over the last 20 years, the incidence of tuberculosis has continued its dramatic fall from pre-World War II levels. Because of this, house officer awareness of the various clinical and roentgenologic manifestations is lessening.1MacGregor RR A year's experience with tuberculosis in a private urban teaching hospital in the postsanitarium era.Am J Med. 1975; 58: 221-228Abstract Full Text PDF PubMed Scopus (64) Google Scholar Recently, two patients were admitted to Montefiore Hospital and Medical Center with abnormal findings on chest roentgenograms, which included bilateral hilar lymphadenopathy; they were found to have tuberculosis. This uncommon roentgenographic finding in adults with tuberculosis is the subject of this communication. A 24-year-old black woman with known sickle cell anemia was admitted to Morrisania City Hospital because of cough, fever, joint pains, night sweats, anorexia, and malaise. Admission physical examination revealed an ill-appearing young woman with blood pressure of 110/70 mm Hg, pulse rate of 100 per minute, respiratory rate of 20 per minute, and rectal temperature of 103.8°F (39.8° C). On cardiac examination she had evidence of cardiomegaly and a grade 2/6 systolic ejection murmur thought to be a flow murmur. Auscultation of her lungs revealed evidence of right lower lobe consolidation. The remainder of her physical examination was unremarkable. Admission laboratory data showed a hematocrit of 27 percent, white blood cell count of 6,500/cu mm with a differential of 42 percent polymorphonuclear leukocytes, 5 percent band forms, and 53 percent lymphocytes. Chest roentgenogram (Fig 1) showed cardiomegaly and bilateral hilar lymphadenopathy with lower lobe infiltrates much more evident in the right hemithorax. The patient was treated for sickle cell crisis with bed rest, hydration, analgesics, and erythromycin. Multiple blood, sputum, and urine examinations for pyogenic and acid-fast organisms were unrevealing. An intermediate strength tuberculin skin test was implanted and was negative after 48 hours. Examinations for mycoplasma, cytomegalovirus, toxoplasmosis and Epstein-Barr virus were all negative and febrile agglutinins, bone survey, lumbar puncture, and a simultaneous liver/lung scan were all noncontributory. A bone marrow biopsy and culture was negative for tuberculosis. Her febrile course continued unabated despite switching antibiotics to high doses of penicillin and kanamycin. She was transferred to Montefiore Hospital and Medical Center for further evaluation. Her chest roentgenogram now showed an increase in the size of the left hilar nodes and the new development of right paratracheal lymphadenopathy. In an attempt to secure tissue for a diagnosis, she underwent fiberoptic bronchoscopy with transbronchial lung biopsy on two occasions, and mediastinoscopy with lymph node biopsy; neither gave a diagnosis. Subsequently, she had an open lung biopsy which showed caseating granulomata in her lung and hilar lymph nodes. Acid-fast bacilli were seen on the Ziehl-Neelsen stains of her lymph nodes and were successfully cultured. A 26-year-old nurse's aide with known S-C hemoglobin disease, was admitted to Montefiore Hospital and Medical Center because of right-sided pleuritic chest pain, cough, fever, abdominal discomfort, diffuse arthralgias, and anorexia. Physical examination showed a slightly obese black woman with blood pressure of 90/60 mm Hg, pulse rate of 92/minute, respiratory rate of 20/minute, and a rectal temperature of 101.2°F (38.4°C). The remainder of the physical examination was non-contributory. Admission laboratory findings showed a hematocrit of 34 percent and a white blood cell count of 8,300 cu mm with a normal differential. Her chest roentgenogram (Fig 2) showed bilateral hilar lymphadenopathy and lower lobe infiltrates, greater on the right. The patient was treated for sickle cell crisis with bed rest, analgesia, and hydration. Multiple sputum, urine and blood cultures for pyogenic organisms were negative, as were the Ziehl-Neelsen stains and cultures of the sputum for acid-fast bacilli. Candida, mumps, and intermediate strength tuberculin skin tests were implanted and all were negative after 48 hours. The patient continued to have a febrile course and on the twelfth hospital day she underwent mediastinoscopy with lymph node biopsy. This showed caseating granulomata. Three days after this procedure, the patient had another intermediate strength tuberculin skin test which now showed 15 mm of induration after 48 hours. Although tuberculosis is a common cause of unilateral hilar or mediastinal lymphadenitis, it infrequently presents as a cause of bilateral hilar lymphadenopathy in adults. The differential diagnosis for this roentgenographic picture most commonly involves sarcoidosis, neoplasms, especially lymphomas, pneumoconioses, and other infectious processes such as coccidioidomycosis and histoplasmosis. Several authors, however, have commented on its infrequent occurrence in adult tuberculous infection. Hodgson et al,2Hodgson CH Olsen AM Good CA Bilateral hilar adenopathy; its significance and management.Ann Intern Med. 1955; 43: 83-99Crossref PubMed Google Scholar in a retrospective survey of 110 patients who presented at the Mayo Clinic with bilateral hilar lymphadenopathy, reported only one patient with tuberculous etiology. Winterbauer et al,3Winterbauer RH Belic N Moores K A clinical interpretation of bilateral hilar adenopathy.Ann Intern Med. 1973; 78: 65-71Crossref PubMed Scopus (207) Google Scholar also in a retrospective study of patients with bilateral hilar adenopathy, found that none of their 100 patients had tuberculous etiology. The only prospective study of note involving bilateral hilar lymphadenopathy was done by Lofgren and Lundbach4Lofgren S Lundbach H The bilateral hilar lymphoma syndrome. A study of the relationship to tuberculosis and sarcoidosis in 212 cases.Acta Med Scandinav. 1952; 142: 265-273Crossref PubMed Scopus (75) Google Scholar in 1952. They surveyed 212 patients who presented with bilateral hilar lymphadenopathy and screened 146 of them for tuberculosis with skin tests and guinea pig innoculations of gastric lavage fluid. They found only one patient with active tuberculosis; the others had sarcoidosis. In the follow-up of up to two years, only one other patient with active tuberculosis was found. Therefore, out of 422 patients with bilateral hilar lymphadenopathy, only two were found to have a definite tuberculous etiology. In 1946, Lofgren5Lofgren A Erythema nodosum: studies on etiology and pathogenesis in 185 adult cases.Acta Med Scandinav Suppl. 1946; 174: 1-197Google Scholar studied 178 adult patients with erythema nodosum to ascertain its relationship to tuberculosis. He noted that 78 of these patients had active tuberculosis and of these 78, 7 (9 percent) had bilateral hilar adenopathy on chest roentgenogram. Twenty years later, Stead et al,6Stead WW Kerby GR Schleuter DP et al.The clinical spectrum of primary tuberculosis in adults.Ann Intern Med. 1968; 68: 731-745Crossref PubMed Scopus (115) Google Scholar studied the clinical and roentgenologic manifestations of 37 adults with primary tuberculosis, 28 of which were proved by culture. They noted unilateral hilar lymph node enlargement in 16 (43 percent), but described only one case of bilateral hilar lymphadenopathy. Weber et al7Weber AL Bird KT Janower ML Primary tuberculosis in childhood with particular emphasis on changes affecting the tracheobronchial tree.Am J Roentgenol. 1968; 103: 123-132Crossref Google Scholar studied 85 children, all with cultureproven tuberculosis. They found that it was much more common to have lymph node enlargement in this group as compared to adults. Eighty of 83 (96 percent) children had regional hilar or paratracheal lymph node enlargement, and 13 of 83 (16 percent) had bilateral hilar enlargement. Both of our patients had a “sickling” hemoglobinopathy and presented with signs and symptoms of sickle cell crisis, thus suggesting the possibility that this disorder may predispose such patients to tuberculous adenopathy or other forms of tuberculosis. The literature8-11 is somewhat controversial in this area, however, and no definitive association has been proved. In conclusion, it should be stressed that the most common etiology for bilateral hilar lymphadenopathy with or without parenchymal infiltrate is sarcoidosis. In our patients, the arthralgias, nonproductive cough, fever, and negative initial tuberculin skin tests all supported this etiology. However, this diagnosis must not be assumed only on the basis of a roentgenographic or clinical picture; other etiologies must sometimes be excluded by lung or mediastinal lymph node biopsy.