Hepatopulmonary Syndrome

repeat sputum examination showed the presence of branching, Gram-positive beaded filaments, which were subsequently recovered on culture and identified as Nocardia asteroides organisms. Intravenous therapy with trimethoprim (20 rug/kg/day) and sulfamethoxazole was begun, and defervescence occurred within 48 h. An enzyme-linked immunosorbent assay was positive for antibodies against the human immunodeficiency virus; this finding was con6rmed by Western blot analysis. T-Iymphocyte subsets revealed an absolute CD4 count of 18 X 1()6!L, with a CD4-CD8 ratio of 0.12. He received two weeks of parenteral therapy and was discharged on oral trimethoprim-sulfamethoxazole and zidovudine. At the three-month follow-up, the patient had no respiratory complaints, and a chest radiograph showed improvement of the upper lobe in6ltrates. This case raises interesting questions concerning the optimal management of pulmonary nocardiosis in patients with AIDS. The treatment of choice for nocardiosis is trimethoprim-sulfamethoxazole," but this recommendation is debated since no increase in efficacy has been observed with this combination over the sulfonamide alone. In vitro studies utilizing clinically achievable concentrations of both drugs have shown synergy with the combination; however, serum levels may not adequately re8ect synergy since there may be increased concentrations of trimethoprim and decreased concentrations of sulfamethoxazole in tissues. Alternative therapies are hampered by the lack of comparison between in vitro activity and clinical outcome. Minocycline has demonstrated clinical efficacy, and in a previous report, an AIDS patient responded initially to the combination of minocycline plus amikacin followed by minocycline plus cycloserine." Newer agents such as imipenem, ceftriaxone, cefotaxime, cefuroxime, and ciprofloxacin have good in vitro activity,· but their role in clinical disease is not defined. The availability of alternative drugs may be particularly important in the AIDS population, in whom adverse reactions to trimethoprimsulfamethoxazole are frequently observed." The duration of treatment for nocardiosis depends on disease site.· For pulmonary involvement, therapy is usually continued for six to 12 months or for two to three months after disease resolution. The length of therapy for AIDS patients is unknown. With the small number of reports of AIDS with nocardiosis, it is difficult to ascertain whether any patients were cured of their Nocardia infection. If duration of treatment for other opportunistic infections in AIDS can be extrapolated to treatment for nocardiosis, it is likely that maintenance therapy may be required following the initial treatment course. Further reports may clarify these issues. Allan R. Tunkel, M.D., Ph.D., john K. Crane, M.D., and Frederick G. Hayden, M.D., Division of Infectious Diseases, University of Virginia School of Medicine, Charlottesville

REFERENCES 1 Kramer MR, Uttamchandani RB. The radiographic appearance of pulmonary nocardiosis associated with AIDS. Chest 1990; 98:382-85 2 Smego RA Jr, Moeller MB, Callis HA. Trimethoprim-sulfamethoxazole therapy for Nocardia infections. Arch Intern Med 1983; 143:711-18 3 Rodriguez JL, Barrio JL, Pitchenik AE. Pulmonary nocardiosis in the acquired immunodeficiency syndrome: diagnosis with bronchoalveolar lavage and treatment with non-sulphur containing drugs. Chest 1986; 90:912-14 4 Gombert ME, Aulicino TM, duBouchet L, Berkowitz LR. Susceptibility of Nocardia asteroides to new quinolones and plactams. Antimicrob Agents Chemother 1987; 31:2013-14 5 Gordin FM, Simon GL, Wofsy CB, Mills J. Adverse reactions to trimethoprim-sulfamethoxazole in patients with the acquired immunode6ciency syndrome. Ann Intern Med 1984; 100:495-99 296

Upper Airway Obstruction Secondary to Aortic Dissection To the Editor:

Upper airway obstruction secondary to aortic dissection is indeed a rare occurrence, as was noted by Giannoccaro et all in the January 1991 issue of Chest. We recently treated a case of a traumatic aortic tear in a 19-year-old man involved in a high-speed motor vehicle collision. When the patient presented to our emergency department, he was sitting up, complaining of difficulty breathing. On examination he was noted to have circumferential swelling of the neck; therefore, he was electively intubated. A chest x-ray film revealed a widened mediastinum. Aortography demonstrated an aortic tear at the isthmus with a pseudoaneurysm and dissection of the hematoma distally as well as proximally into the neck. Emergency thoracotomy confirmed the diagnosis, and aortic replacement was successfully accomplished. The patient was returned to the operating room and extubated without incident on the second postoperative day. In this patient with a life-threatening aortic tear, airway obstruction due to dissection of the hematoma was the only symptom in an otherwise-asymptomatic patient. This case again illustrates that aortic pathology should be suspected in patients presenting with airway obstruction and neck swelling. Dominick Cadaleta, M.D., Roy Nelson, M.D., F.C.C.R, and Andmv Sa1OO, M.D., Department of Surgery, North Shore University Hospital, Manhasset, New York

REFERENCE 1 Giannoccaro PJ, Marquis JF, Chan KL, Walley ~ Chambers RJ. Aortic dissection presenting as upper airway obstruction. Chest 1991; 99:256-58

Hepatopulmonary Syndrome 'Ib the Editor: In our November 1990 editorial in Chest, I we indicated that the term "hepatopulmonary syndrome" was probably first suggested by Eriksson and colleagues" in 1988. However, in an article published in Chest in 1977, Kennedy and Knudson" actually suggested the term, as well as the potential reversibility of the condition. We wish to recognize this earlier publication, as well as our unintentional oversight of the authors' prior use of the term. Michael] Krmoka, M.D., F.C.C.R, Mayo Clinic jacksonville, ]ackscmville, Florida, and Denis A. Cortese, M.D., F.C.C.R, Mayo Clinic, Rochester, Minnesota

REFERENCES 1 Krowka MJ, Cortese DA. Hepatopulmonary syndrome (editorial). Chest 1990; 98:1053-54 2 Eriksson LS, Soderman C, WOOren J, Ericzon BC, Eleborg L, Hedenstierna G. Is hypoxemia in cirrhotic patients due to a functional "hepatopulmonary" syndrome? J Hepatol 1988; 7(suppl):529 3 Kennedy TC, Knudson RJ. Exercise-aggravated hypoxemia and orthodeoxia in cirrhosis. Chest 1977; 72:305-9 Communications to the Editor